Spinal Imaging ( DX-Direct )

Direct Diagnosis in Radiology

Spinal Imaging Professor Herwig Imhof, MD Department of Radiology Division ofOsteoradiology Medical University Vienna Vienna General Hospital (AKH) Vienna. Austria With contributions

by

Benjamin Halpern, Andreas M, Herneth, Klaus M, Friedrich, Michael Matzner, Christina Mueller-Mang, Iris-Melanie Noebauer-Huhmann, Daniela Prayer, Oliver Sommer, Florian Wolf

327 Illustrations

Thieme Stuttgart, New York

Library of Congress Cataloging-in-Publication

Data

Wirbelsaule. English. Spinal imaging I [edited by] Herwig Imhof: with contributions by Benjamin Halpern . let al.: translaror: John Grossman: illustrator, Emil Wolfgang Hanns). p.:cm. Includes bibliographical references and index. 15BN97B-3-13-144071-6 15BN97B-I-58890-560-4

(TPS : alk. paper)(TPN : alk. paper)

1. Spine-Imaging. 2. Spinal cord-Imaging. 3. Spine-Diseases-Diagnosis.4. Spinal cord-Diseases-Diagnosis. I. Imhof, H. (Herwig) II. Halpern, Benjamin. III.Title. (DNlM: I. Spinal Diseases-diagnosisHandbooks. 2. Diagnostic Imagingmethods-Handbooks. 3. Spinal Cord Diseases-diagnosis- Handbooks. WE 39 W798s 2007a) RD768.W5513 2007 617.4'8207548-dc22

2007023541

This book is an authorized and revised translation of the German edition published and copyrighted 2006 by GeorgThieme Verlag. Stuttgart. Germany. Title of the German edition: Pareto-Reihe Radiologie: Wirbelsaule. Translator: John Grossman. Schrepkow, Germany Illustrator: Emil Wolfgang Hanns. Schriesheim. Germany It> 2008 Georg Thieme Verlag KG RGdigerstrasse 14,70469 Stuttgart, Germany http://www.thieme.de Thieme New York.333 Seventh Avenue, New York, NY 10001. USA

http://www.thieme.com Cover design: Thieme Publishing Group Typesetting by Ziegler + MOiler. Kirchentellinsfurt. Germany Printed by APPl. aprinta Druck, Wemding. Germany ISBN 978-3-13-144071-6 (TPS, Rest of World) ISBN 978-1-58890-560-4

(TPN.The Americas)

123456

Important note: Medicine is an ever-changing sciE:'nce undergoing continual development. Research and clinical experience are continually expanding our knowledge. in particular our knowledge of proper treatment and drug therapy. Insofar as this book mentions any dosage or application. readers may rest assured that the authors. editors. and publishers have made every effort to ensure that such references are in accordance with the state of knowledge at the time of production of the book. Nevertheless. this does not involve, imply. or express any guarantee or responsibility on the part of the publishers in respect to any dosage instructions and forms of applications stated in the book. Every user is requested to examine carefully the manufacturers' leaflets accompanying each drug and to check. if necessary in consultation with a physician or specialist. whether the dosage schedules mentioned therein or the contraindications stated by the manufacturers differ from the statements made in the present book. Such examination is particularly important with drugs that are either rarely used or have been newly released on the market. Every dosage schedule or every form of application used is entirely at the user's own risk and responsibility. The authors and publishers request every user to report to the publishers any discrepancies or inaccuracies noticed. If errors in this work are found after publication. errata will be posted at www.thieme.com on the product descri ption page. Some qf the product names, patents, and registered designs referred to in this book are in fact registered trademarks or proprietary names even though specific reference to this fact is not always made in the text. Therefore. the appearance of a name without designation as proprietary is not to be construed as a representation by the publisher that it is in the public domain. This book. including all parts thereof, is legally protected by copyright. Any use, exploitation. or commercialization outside the narrow limits set by copyright legislation. without the publisher's consent, is illegal and liable to prosecution. This applies in particular to photostat reproduction, copying, mimeographing, preparation of microfilms. and electronic data processing and storage.

Benjamin Halpern, MD Department of Radiology Division ofOsteoradiology Medical University Vienna Vienna General Hospital (AKH) Vienna, Austria

Iris-Melanie Noebauer-Huhmann, Department of Radiology Division ofOsteoradiology Medical University Vienna Vienna General Hospital (AKH) Vienna, Austria

Andreas M. Herneth, MD Professor Department of Radiology Division ofOsteoradiology Medical University Vienna Vienna General Hospital (AKH) Vienna. Austria

Daniela Prayer, MD Professor Department of Radiology Division of Neuroradiology Vienna General Hospital (AKH) Vienna, Austria

Klaus Friedrich, MD Department of Radiology Division of Osteoradiology

Oliver Sommer, MD Central Department of Radiology Lainz Hospital

Medical

Vienna, Austria

University

Vienna

Vienna General Hospital (AKH) Vienna, Austria Michael Matzner, MD Department of Orthopedics Medical University Vienna Vienna General Hospital (AKH) Vienna, Austria

Medical

University

MD

Vienna

Florian Wolf, MD Department of Radiology Division of Osteoradiology Medical University Vienna Vienna General Hospital (AKH) Vienna. Austria

Christina Mueller-Mang, MD Department of Radiology Division of Neuroradiology Medical University Vienna Vienna General Hospital (AKH) Vienna. Austria

v

Congenital Malformations Christina Mueller-Mang, Daniela Prayer, Klaus M. Friedrich, Michael Matzner

Arnold-Chiari Malformation 1 Lumbarization and Sacralization .. 4 Diastematomyelia 6 Tethering 9 Sacrococcygeal Teratoma 13 Meningocele, Myelomeningocele. 16

2

Vertebral Malformations Klippel-Feil Syndrome Kyphosis Scheuermann Disease Scoliosis Malrotation

21 26 29 33 36 40

Trauma Christina Mueller-Mang,

Daniela Prayer. Klaus M. Friedrich, Florian Wolf,

Michael Matzner. Herwig Imhof

Spinal InjuryMagerl Classification Vertebral Fractures-Causes Dens Fracture Flexion Fracture of the Cervical Spine Burst Fracture of the Spine Chance Fracture (Seat8eltFracture) Jefferson Fracture

3

43 45 48 51 54 58 60

Hangman's Fracture Spinal Cord Trauma Syringohydromyelia Anterior Subluxation Insufficiency Fracture ofthe Sacrum Stress Phenomena in the Spine Stress Fractures in Ankylosing Spondylitis

63 66 69 73 76 79 83

Degenerative Disorders Iris-Melanie Noebauer-Huhmann, Benjamin Halpern, Michael Matzner, Herwig Imhof

Disk Degeneration Degenerative Disk DiseaseModic I Degenerative Disk DiseaseModicll Spondylosis DeformansModiclll Disk Herniation Bulge, Protrusion, Extrusion, Sequestration Disk Calcification and Vacuum Phenomenon ,

VI

87 90 93 96 100 103 108

FacetJoint Degeneration UncovertebralOsteoarthritis Synovial Cyst Hypertrophy of the Ligamenta Flava Baastrup Disease Spondylolisthesis and Pseudospondylolisthesis Degenerative Spinal Stenosis Diffuse Idiopathic Skeletal Hyperostosis

111 116 118 120 121 123 126 131

Contents 4

Inflammatory Disorders Christina Muelfer-Mang, Daniela Prayer, Andreas M. Herneth, Oliver Sommer, Michael Matzner, Herwig Imhof

Rheumatoid Arthritis .... Rheumatoid ArthritisChronic Trauma Psoriatic Spondyloarthropathy Reiter Syndrome Ankylosing Spondylitis Ankylosing SpondylitisLigament Calcification and Bamboo Spine ..... Ankylosing SpondylitisFractures

5

133 138 141 144 147

IS8 166 172 17S 178 182 186

IS2 IS4

Tumors Andreas M. Herneth. Christina Muefler-Mang. Daniela Prayer, Michael Matzner. Herwig Imhof

Hemangioma Osteoid Osteoma Osteoblastoma Osteochondroma Aneurysmal Bone Cyst Giant Cell Tumor Langerhans Cell Histiocytosis MalignantTumors Bone Metastases Multiple Myeloma

6

Acute Bacterial Spondylitis .. .... Tuberculous Spondylitis Epidural Abscess . Granulomatous Inflammations of the Spinal Cord . Arachnoiditis . Acute Transverse Myelitis . Spinal Multiple Sclerosis .

190 195 198 201 204 208 212 215 216 222

Chordoma Ewing Sarcoma ............•.•..... Lymphoma Nerve Sheath Tumors Leptomeningeal and Intramedullary Metastases Meningioma Ependymoma Astrocytoma Hemangioblastoma

226 229 232 237 240 244 248 252 256

Vascular Disorders Christina Mueller·Mang. Daniela Prayer

Epidural Hematoma Arteriovenous Malformation Arterial Spinal Cord Infarction

..

259 262 266

VII

7

Postoperative

Disorders

Andreas M. Herneth,

Michael Matzner,

Failed Back Surgery Syndrome CSFFistula Peridural Fibrosis

8

..

270 272 27S

Herwig Imhof

Rapidly Progressive Osteoarthritis (After Intersegmental Fusion) .... Complications of Spinal Instrumentation

277 280

Metabolic Disorders Andreas M. Herneth. Herwig Imhof

Senile and Postmenopausal Osteoporosis

Index

VIII

287

29S

Paget Disease Spinal Epidural Lipomatosis

291 293

ACE

Angiotensin converting

HIV

enzyme ADEM AFP A-P AVF c-ANCA CSF CT DO DEXA DISH DSA OWl FOG-PET

Acute disseminated encephalomyelitis Alpha-fetoprotein Anterior-posterior Arteriovenous fistula Cytoplasmic antineutrophil cytoplasmic antibody Cerebrospinal fluid Computed tomography, computed tomogram Differential diagnosis Dual-energy x-ray absorption Diffuse idiopathic skeletal hyperostosis Digital subtraction angiography Diffusion-weighted imaging Fluoro-18-deoxyglucose positron emission tomography

MRI NSAID P-A PCR PO PET PNET Q-CT SPECT STIR TNF-a TSE

Human immunodeficiency virus Magnetic resonance imaging Nonsteroidal antiinflammatory drug Posterior-anterior Polymerase chain reaction Proton density Positron emission tomography Primary neuroectodermal tumor Quantitative cr Single photon emission computed tomography Short tau inversion recovery Tumor necrosis factor Ci Turbo spin echo

IX

Definition ~ Epidemiology Rare malformation of the posterior cranial fossa and craniocelVical junction (underdevelopment of the endochondral occiput) • Autosomal inheritance pattern. ~ Etiology, pathophysiology, pathogenesis Chiari I: Displacement of the cerebellar tonsils caudal to the foramen magnum (McGregor line) • Associated with cervical syringomyelia (syringohydromyelia) and atlantooccipital fusion (25-50% of cases) • May occur in combination with scoliosis and kyphosis (42% of cases). Chiari II: Small posterior cranial fossa. Portions of the cerebellum. fourth ventricle. and medulla oblongata are caudally displaced. Hypoplastic pons associated with spinal dysraphism (most often lumbar myelomeningocele). Chiari III: Very rare. Type II malformation combined with an occipital or high cervical encephalocele. Chiari IV: Very rare. Aplasia or severe hypoplasia of the cerebellum. Small brainstem • Enlarged CSF spaces in the posterior cranial fossa. Cautian: In published literature, the term "Arnold-Chiari" is used for both Chiari I and Chiari II malformations.

Imaging Signs

............................................................................................ ~ Modality of choice - MRI: Sagittal. Axial. CSF flow measurement (Chiari I). - Prenatal ultrasound or fetal MRI. ~ MRI findings Chiari I: Descent of the cerebellar tonsils (> 5 mm caudal to the foramen magnum) • Malformation of the bony skull base is common (shortened clivus) • The fourth ventricle appears normal or elongated. The posterior cranial fossa

is not too small. There are no associated cerebral malformations. Secondary hydrocephalus may result from blockage of CSF drainage in the foramen magnum • Syringomyelia is present in 50-75% of cases. Abnormal CSF pulsation (CSF flow measurement). Chiari II: Early diagnosis on fetal MRI (associated malformations) • Closed or open dysraphism (more often lumbar than cervical) • Portions of the cerebellum and medulla oblongata are displaced into the spinal canal. Hypoplasia of the posterior cranial fossa with parietooccipital microgyria. Callosal dysgenesis· Hypoplastic. flattened pons. Enlargement of the prepontine cisterns. Beaklike extension of the quadrigeminal plate. Hydrocephalus. Syringomyelia (hydromyelia) extending past C1. ~ Prenatal and postnatal ultrasound findings Chiari II: Caudal displacement of the cerebellum. Hydrocephalus.

Arnold-Chiari Malformation Fig. 1.1 A 57-year-old man with a history of pain in both upper extremities for many years, now accompanied by sensa· ry deficits on the left side. MR image of the craniocervical junction (sagittal, T2). The image shows elongation and cervical descent of the cerebellar tonsils accompanied by cervical hydromyelia (ArnoldChiari I).

Fig.1.2 Fetal MR image (sagittal. T2. single-shot fast-spin echo). A small posterior cranial fossa with caudal displacement of the cerebellum, enlarged ventricles. and lumbar myelomeningocele (Chiari II).

2

Arnold-Chiori Molformotion Clinical Aspects ............................................................................................ • Typical presentation Chiari I: Up to 50% of all cases are asymptomatic. Herniation> 12 mm is almost invariably symptomatic. Pain on movement of the head and neck. Gait ataxia. Caudal cranial nerve symptoms. Sleep apnea. Chiari II: Myelomeningocele. Paralysis of the lower extremities. Sphincter dysfunction. Obstructive hydrocephalus. Brainstem compression . •.. Therapeutic options Chiari I: Patients with symptoms require suboccipital craniotomy or dorsal resection ofC1 to decompress the spinal cord. Conservative treatment is indicated in the absence of syrinx. Chiari II: Hydrocephalus is treated by shunting. Surgical closure of the myelomeningocele (sometimes this may be done prenatally, in which case there will be near normal development of the posterior cranial fossa).

Differential Diagnosis ............................................................................................ Acquired hydromyelia cause

from anather

Descent af the cerebellar tonsils

- Basilar invagination (osteogenesis imperfecta. Paget disease. acromegaly, Klippel-Feil syndrome) - Chronic petrosal vein shunt, elevated intracranial

pressure Selected

References

Gammal TE, Mark EK. Brooks BS. MR imaging of Chiari II malformation. Am J R5nrgenol 1988: 150: 163-70 Osborn AG. Diagnostic Neuroradiology. Philadelphia: Mosby 1994: 15-24.66

3

Definition (Tronsitional Lumbosacral Vertebra) ............................................................................................ Sacralizatian: The border between the sacrum and lumbar spine is shifted one segment cranially. Lumbarization: The first sacral vertebra develops as a lumbar vertebra. Cranial

shifts are more common

than lumbarization.

Sacralization

can also occur

unilaterally. A full-spine radiograph is required to clearly identify the malformation as lumbarization or sacralization. Wherever this is not feasible or not indicated. the term "transitional lumbosacral vertebra" is preferred. Imaging Signs ............................................................................................ ~ Modality of choice - Conventional radiographs or CT. - MRI(when neurologic symptoms are present). Clinical Aspects ............................................................................................ ~ Typical presentation Asymmetric

transitional

lumbosacral

vertebrae.

in particular,

are often accom-

panied by spinal symptoms. ~ Therapeutic options Physical therapy. Selected References Brossmann J. Czerny C, Freyschmidt J. Crenzen des Normalen und Anf.:inge des Pathologischen in der Radiologie des kind lichen und erwachsenen Skeletts. 14th ed. Stuttgart:

Thieme 2001

4

Lumbarization

and Sacralization

Fig. 1.3 Conventional radiograph of the lumbosacral junction (A-P. detail). Asymmetrical transitional lumbosacral vertebra.

Fig. 1.40. b

Schematic diagram: Sacralization (a): lumbarization (b).

5

Definition ............................................................................................ •

s: Q ~

3

...• o' :l Q

'"

Epidemiology

Rare closed spinal dysraphism • Most common in the lumbar and thoracic spine. More common in men than in women (4: 1). • Etiology, pathophysiology, pathogenesis Characterized by development of a sagittal cleft in the spinal cord. Type I (diastematomyelia with a septum): The spinal cord is split by a bony or cartilaginous septum or "spur" extending between the vertebral body and arch. Each hemicord has its own dural tube and separate subarachnoid space. The hemicords may be asymmetrical. Type 11(diastematomyelia without a septum): The two hemicords are contained in a single dural tube. occasionally separated by a fine cartilaginous septum. Cutaneous stigmata: Hypertrichosis. hemangioma. lipoma. dermal sinus. Associated with bony malformations (85% of cases): Fused vertebrae. hemivertebrae, "butterliy" vertebrae. scoliosis (up to 60% of cases) • Associated hydromyelia (30-40% of cases). especially with type I • Associated myelomeningocele. Imoging Signs ............................................................................................ •

Modality of choice

MRI: - Sagittal: TI, T2 (skin surface also visualized). - Coronal: With severe scoliosis.

- Transverse: T2-TSEwith 3-mm slice thickness in the region of the bony defects. slice thickness of 5- 10 mm over the rest of the spinal cord (associated hydromyelia); TI with 3-mm slice thickness over the bony defects. - Contrast administration

is indicated when intraspinal 50ft tissue components

are present (cartilaginous structures can develop into fibromatous tumors) or for postoperative imaging (to exclude inliammation): Sagittal and transverse TI-weighted sequences with fat suppression. - Cerebral MRIto identify associated anomalies. •

MRI findings The two hemicords are visualized with their common or separate dural tubes

and/or a bony spur. Associated hydromyelia or adherent lipomas are seen. Vertebral dysplasia is visualized. The precise craniocaudal extent of the malformation is seen. Prenatal examination is also possible. • Cffindings

Three-dimensional visualization of the bony anomalies. Cf myelography can demonstrate the cleft spinal cord when MRIis contraindicated. Useful for visualizing associated bony malformations and reconstruction in all planes. • Ultrasound

findings

Prenatal diagnosis and postnatal examination through the bony aperture. • Conventional

radiography

findings

A bony spur and vertebral dysplasia may be seen. 6

Diastematomyelia Rg. 1.5 A 25-year-old patient with a history of scoliosis since childhood pre· sented with increasing sensory deficits and weakness in the right hand. and beltlike bands of pain. MR image of the cervicothoracic region (coronary. T2). Two narrow hemicords are separated by a bony septum (type I diastematomyelia with septum).

Fig.I.6 MR image of T1 (axial. GRE). Hemicords are visualized. Adhesions to the bony septum are seen on the right.

7

Diastematomyelia Clinical Aspects ~ Typical presentation Often only becomes symptomatic in adults. Scoliosis. Discrete atrophy or weakness in one or both lower extremities. Progressive paraparesis. Bladder and bowel dysfunction. ~ Therapeutic options Surgical intervention immediately after the diagnosis to avoid irreversible damage to the nerve tissue. Resection of a bony spur or fibrous septum. Correction of a tethered cord. Differential Diagnosis ............................................................................................ Hydromyelia

- May present a similar picture where axial and coronal slices are not obtained

Selected References Pang 0 et al. Split cord malformation. Part I: A unified theory of embryogenesis for double

spinal cord malformations. Part II: Clinicalsyndrome. Neurosurgery 1992: 31: 214217.481-500 Songio-Cohen Pet al. Prenatal diagnosis of diastematomyelia. Childs Nerv Syst 2003; 19:

555-566 Tartori-Donati Pet al. Magnetic Resonance Imaging of Spinal Dysraphism. Topics Mag Res

1m2001: 12: 375-409

8

Definition • Epidemiology Almost always congenital. Most commonly occurs in preadolescence (7-12 years) • Predilection: lumbosacral region. • Etiology. pathophysiology, pathogenesis "Tethered cord" is not a morphologic symptom but a clinical syndrome consistingof: - Pain and/or sensory deficits in the lower extremity. - Spastic gait. - Muscle atrophy. - Occasionally bladder and bowel dysfunction. - Occasionally club foot. • Etiology Adherence of the spinal cord to the dura prevents the cord from ascending normally and results in increasing traction. Intradural lipoma or lipomyelomeningocele. Split cord malformation (diastematomyelia) • Dermal sinus. Fibrotic lipomatosis ("fatty filum") • Myelomeningocele. Arachnoiditis. Posttraumatic condition.

s:

Q

-a-..,

3 Q

o::>' '"

Imaging Signs

............................................................................................ • Modality of choice MRI: - Sagittal: n. T2 (skin surface also visualized). - Coronal: With severe scoliosis. - Transverse: T2-TSEwith 3-mm slice thickness in the region of the bony defects • Slice thickness of 5-10 mm over the rest of the spinal cord (associated hydromyelia. diastematomyelia: n with 3-mm slice thickness over the bony defects). - Contrast administration

is indicated where intraspinal soft tissue components

are present (cartilaginous structures can develop into fibromatous tumors) or where there is postoperative inflammation:

Sagittal and transverse T1-

weighted sequences with fat suppression. - Cerebral MRIto exclude associated malformations. - CSFflow study. - Fetal MRI:To assess the prognosis.

9

Tethering Fig.l.7 A 4-year-old boy with spastic gait and bladder dysfunction. MR image of the lumbar spine (sagittal. T2). There is no typical conus medullaris. the spinal cord is elongated and fixed within a lipoma at the level of 52.

Fig.I.8 MR image of the lumbar spine (sagittal, T1). Lipoma fused with the short, thick fibers of the cauda equina ("thickened fatty filum").

10

Tethering Fig.l.9 MRI of 51 (axial. T1). Neural structures are fixed within the lipoma.

•

MRI findings Descent of the conus medullaris (normal position at 8-10 weeks after birth is approximately L1-L2) • Changes in the shape of the conus medullaris: Elongated and thinned without the physiologic bulb-shaped expansion of the spinal cord at the level of the conus medullaris • Filum tenninale: Thickened and shortened. Underlying pathology is visualized. • CTfindings Three-dimensional reconstruction to visualize associated bony malformations. Urodynamic study. Evaluation of compromised bladder function. IT myelography: Evaluation of descent of the conus medullaris when MRI is contraindicat-

ed. •

Ultrasound findings Fetal examination to assess prognosis. In the presence of instability in a newborn (when MRI is not feasible) • Prenatal detection of dysraphism • Direct visualization of tethering (through a bone aperture after a laminectomy). • Radiographic findings Visualization of ossocioted bony onomalies: Spina bifida. fused vertebrae. rib malformations. Evaluation of scoliosis.

II

Clinical Aspects

............................................................................................

• Typical presentation Increasing muscle weakness. Heightened muscle tone. spasticity. Unsteady gait. Rapidly progressive scoliosis. Increasing bladder and bowel dysfunction. Back and leg pain. Leg deformity .

• Therapeutic options Surgical intervention is indicated only in worsening neurologic symptoms or pain resistant to therapy. Primary goal: Prevention of further neurologic deficits; postoperative improvement of neurologic function is a secondary aim that is often not achieved. Mobilization of the fixed spinal cord. Resection of scar tissue. Laminectomy where indicated. Surgical complication rate: 1-2% (infection. bleeding. worsening of neurologic symptoms). Tethering recurs in 10-20% of all cases. especially where the initial surgery is performed at an early age (growth of spinal column).

Differential Diagnosis Drop metastases

- History (underlying malignancy) - Difference in patient age

Assodated malJonnatians with tethering Selected

Refetences

(ornette Let at. Closed spinal dysraphism: a review on diagnosis and treatment in infancy. Eur J Paediatr Neural 1998: 2: 179-185 Gupta SKet al. Tethered cord syndrome in adults. Surg Neural 1999: 52: 362-370 Kim MJ et al. Tethered spinal cord with double spinallipomas.J Korean Med Sci 2006: 21: 1133-1135 SarwarkJF et al. Tethered cord syndrome in low motor level children with myelomeningocele. Pediatr Neurasurg 1996; 25: 2 Yamada S. Won OJ.What is the true tethered cord syndrome? Childs Nerv Syst 2007: 23: 371-375

12

Definition ............................................................................................ • Epidemiology Most common congenital neoplasm, usually diagnosed before birth. Benign in 80-85% of cases. Mortolity: 15-35% • Localizarion: Lesions are usually intradural and extramedullary, rarely intramedullary (2% of cases) • More common in females than males (3:1); malignant subtype is more common in males, • Etiology, pathophysiology, pathogenesis Mixed tumor with tissue components from all three germ layers. Arises from pluripotent cells of the node of Hensen. The tissue components exhibit varying degrees of maturation, Staging classification: - Type I: Spreads beyond the fetus, - Type II: External and presacral spread, - Type III: Small external component, primarily intrapelvic and intraabdominal tumor spread, - Type IV;Completely presacral tumor, Currarino rriad: - Sacral anomaly, - Anal atresia or stenosis.

- Presacral rumor (benign teraroma in 40% of all cases, anterior meningocele in 47%),

Imaging Signs ............................................................................................ • Modality of choice MRI: - Sagitral: Tt, T2, STIR. - Coronal: T2, - Axial: T2, Abdominal study (CTor MRI): Evaluation of ventral spread (into the abdominal cavity), II>-

General

Inhomogeneous solid-cystic mass in the region of the sacrum and distal lumbar regions. Secondary hydronephrosis due to compression. Polyhydramnios, • MRI findings Cysts: Homogeneously hyperinrense (Tt and T2) with high protein content, or hypointense (Tt) and hyperintense (T2) with serous content, occasionally septate. Solid nodules: Enhance with contrast. Fatty components: Fat suppression with a STIRsequence. Calcified deposits: Markedly hypointense on Tl and T2, • Ultrasound findings Hyperechoic (solid) areas with inclusions of or peripheral anechoic (cystic) comspine. occasionally extending into the intrapelvic and intraabdominal

ponents • Calcifications: Hyperechoic foci with acoustic shadows.

13

Sacrococcygeal Teratoma Fig.I.IO Newborn with a known a sacrococcygeal mass detected by prenatal ultrasound. Pelvic MR image (sagittal. T2). Mass with a larger component anterior to the spine than posterior to the spine. exhibiting inhomogeneous signal; the caudal spine is completely present.

MR image of the sacrum (coronal. T2). Tumor spread is visible in the sacrum. Fig. J.JI

14

Sacrococcygeal Terotama

Clinical Aspects ............................................................................................ • 1)tpicaJ presentation Hydrops/etalis: Results from intrauterine complications such as polyhydramnios and tumor hemorrhage. Fatal prognosis where hydrops occurs prior to the 30th week of pregnancy (93% mortality) • Postpartum morbidity resulting from associated congenital anomalies (10% of cases), compression of adjacent organs (such as the urogenital tract), recurrent tumor, intraoperative and postoperative

complications . • Therapeutic options In cases of hydrops, birth should be induced as soon as the lungs are sufficiently mature. Radical resection of the tumor including the coccyx is indicated prior to birth or within the first week of life. Fetal interventions: Tumor resection, cyst aspiration. reduction of the amnion.

Differential Diagnosis

............................................................................................ Extemol tumors: myelomeningocele Intrapelvic tumors

- Spina bifida located higher and further dorsal

- Ovarian. mesenteric cysts - Bowel dilation or duplication - Cystic neuroblastoma

Solid tumors

-

Chordoma Neurogenic tumors Lipoma Hemangioma Malignant melanoma

Selected References Avni FEet al. MR imaging of fetal sacrococcygeal teratoma: diagnosis and assessment. AJR AmJ Roentgenol2002; 178: 179-183 Feldman M et al. Neonatal sacrococcygeal teratoma: multiimaging

modality assessment.

J Pediatr Surg 1990: 26: 675-678 Hedrick HL et al. Sacrococcygeal teratoma:

prenatal assessment, fetal intetvention.

and

outcome.J Pediarr Surg 2004: 39: 430-438

15

Definition Spinal dysraphism: Developmental anomaly with incomplete closure of the neural

tube. A third of dysraphic anomalies are open and two-thirds are closed. Meningocele: Accounts for 2.4% of all closed dysraphic anomalies. Herniation of a CSF-filled sac lined with dura and arachnoid through a posterior spina bifida • Completely covered by skin. Incomplete dysraphism with incomplete closure of the vertebral arch (spina bifida) is common. Often there is associated superficial skin pathology (indentation, hypertrichosis, etc.) • Spina bifida is usually clinically insignificant.

Lesion usually does not contain any nerve structures (rarely nerve

roots of the filum terminale will pass through a large meningocele). Not an indication for immediate surgery. Meningomyelocele: Most common type of open spinal dysraphism (98.8% of cases). Herniation of the incompletely developed spinal cord and meninges through a bony defect in the posterior vertebral structures with projection of these neural structure above the surface of the skin (neural placode) • Often combined with an abnormally small posterior cranial fossa, caudal herniation of cerebellar tissue, and hydrocephalus (. Chiari II malformation) • Imaging studies are useful primarily for postoperative follow-up and visualizing associated malformations; hydrocephalus in the setting of a Chiari IImalformation may develop only after closure of the meningomyelocele. Neurosurgical emergency: Surgical closure is indicated within 48 hours to avoid infection of the exposed spinal cord and an increase in neurologic dysfunction. Lumbar and lumbosacral regions are most often affected • More common in women than in men. Imaging Signs

• Modality of choice MRI: - Sagittal: TI, TI (skin surface also visualized). - Coronal: With severe scoliosis. - Transverse: TI-TSE with 3-mm slice thickness in the region of the bony defects. Slice thickness of 5-10 mm over the rest of the spinal cord (associated hydromyelia, diastematomyelia); TI with 3-mm slice thickness over the bony defects. - Contrast administration is indicated when an intraspinal soft tissue component is present (cartilaginous structures can develop into fibromatous tumors) or when there is postoperative inflammation: Sagittal and transverse

Tl-weighted sequences with fat suppression. - Cerebral MRIto exclude associated malformations. - CSFflow study where tethering is suspected. - Fetal MRI:To assess the prognosis.

16

Meningocele,

Myelomeningocele

Fig, 1.12 Conventional radiograph of the

lumbosacral junction (A-P, detail). Spina bifida at LS.

Fig.I.l3 Findings at birth included a sacral mass. Motor function in the child's legs was normal. MR image of the lurn· bosacral region (sagittal, 12). Myelocele sac containing CSFbut otherwise empty. Intraspinal descent of the conus medullaris with short straight cauda equina fibers that are fixed to the caudal end of the dural sac.

17

Meningocele. Myelomeningocele Fig.1.14 MR image of lS (axial. T2). Bony defect is occluded by a connective tissue structure (operative report) through which a (SF-filled sac has herniated. Septa are present but there are no neural structures. These structures lie entirely within the spine. The anterior (SF spaces are not enlarged. The myelocele sac is covered by a thin layer of skin along its margins.

Fig.I.IS Ultrasound examination in the 20 th week of pregnancy detected spina bifida. MR image of the fetus and pelvis (coronal, 12). Sacral myelocele sac with neural structures coursing along its apex. The axial T2-weighted sequence shows the broad-based bony defect and neural structures within the myelocele (arrow).

18

Meningocele. Myelomeningocele • MRI findings Clinical indication. Preoperative evaluation. Anatomic characterization of the constituent components of the malformation and their relation to the nerve roots. Identification of morphology and entity. Identification of coexisting diastematomyelia

(such as hemimyelomeningocele)

• Postoperative visualization

of complications • Hydrocephalus: 48-72 hours postoperatively • Recurrent tethering: Strands of scar tissue fix the spinal cord to the dura. Arachnaid cysts: Sequela of postoperative adhesions. Slightly hyperintense to CSF(elevated protein content) • Fine wall. No flow artifacts in contrast with CSF• Dennaid and epidermoid cysts: Occur as a result of intraoperative inclusion of epidermal cells. as a primary lesion. or in association with a dermal sinus. Slightly hyperintense to CSF on Tl- and T2-weighted images. Superinfection enhances with contrast. Caution: Rupture leads to toxic meningitis. Syringomyelia (syringahydramyelia): Primarily responsible for worsening postoperative neurologic symptoms. leads to rapidly progressive clinical scoliosis. • CTfindings Three-dimensional

reconstruction to visualize associated bony malformation.

• Conventional radiographs Visualization of bony defect (spina bifida) • Evaluation of scoliosis. • Ultrasound findings Prenatal detection of dysraphism • Fetal ultrasound to assess the prognosis. To evaluate the conus medullaris and filum terminale in newborns with instability (where MRIis not feasible) • Amniocentesis. Elevated AFP.

Clinical Aspects

............................................................................................ • Typical presentation Meningacele: Usually clinically asymptomatic (no primary spinal cord lesion) • Caution: Pressure sores can ulcerate to form open lesions. Tethered cord syndrome with progressive neurologic symptoms. Meningomyelacele: Reddish raised exposed nerve tissue in the middle of the

back. Sensorimotor deficits in the lower extremity. Bladder and bowel dysfunction. Rarely psychomotoric retardation. Severity of the different symptoms varies . •.. Therapeutic options Meningacele: Immediate closure of the meningocele where ulcerating pressure sores are present. Elimination of a tethered cord syndrome. Meningomyelocele: Neurosurgical emergency • Mobilization of the placode •

Closure of the soft tissue defect.

Fetal surgical procedures are being tested.

19

Differential

Diagnosis

............................................................................................

Open spinal dysraphism

- Myeloschisis (- myelocele): Very rare. Because the

Closed spinal dysraphism

-

-

subarachnoid space does not extend to the level of the defect, the neural placode lies at skin level or slightly recessed. Hemicord with myelocele or myelomeningocele: Malformation affects only one hemicord Lipomyeloschisis: Subcutaneous intraspinal lipoma adhering to the neural placode Lipomyelocele: Subcutaneous extraspinallipoma adhering to the neural placode Lipomyelomeningocele: Subcutaneous lipoma. usually adhering asymmetrically to the neural placode. Myelocele on the contralateral side Terminal myelocystocele: Central canal expanded to form a terminal cyst (syringocele) Cervical myelocystocele: Dorsal wall of the central canal is displaced and communicates

with a menin-

gocele - Cervical myelomeningocele: Fibrous neurovascular cord is displaced into a meningocele through a posterior wall defect Selected References Rossi A et al. Imaging

in spine and spinal cord malformations.

Eur

J

Radiol 2004:

50:

177-200 Schijman E. Split cord malformation:

report of 22 cases and review of literature.

Childs

Nerv Syst 2003; 19: 106-108 Tenori-Donati

Pet al. Magnetic Resonance Imaging of Spinal Dysraphism. Topics Mag Res

1m2001; 12: 375-409

20

Definition ............................................................................................ Partial or complete malformation of the vertebrae. Abnormal vertebral segmentation and fusion. Total aplasia: Absence of both ossification centers. Very rare. Lateral hemivertebra: Failure of ossification of one of the two ossification centers. A distinction is made between the primordium of a hemivertebra exhibiting a verte-

bral arch of normal length (hemisoma) and the primordium of a hemivertebra with half an arch (hemispondylus). This is often associated with scoliosis and deformities of the bony thorax. Butterfly vertebra (partial ventral or dorsal cleavage): Failure of fusion of the individual ossification

centers.

Persistent notochord: The remnant divides the vertebral body into two halves: the clefts of the ventral and dorsal halves extend to the notochord canal. Total sagittal cleavage: This very rare deformity is incompatible with life. Congenitally fused vertebrae: Partial or total fusion of adjacent vertebrae due to failure of segmentation; partial fusion anomaly type A: Fusion in the anterior third of the vertebral body; type B: Fusion in the posterior third of the vertebral body with or without fusion of the vertebral arches and facet joints. Imaging Signs ~ Modality of choice

- MRI: Multiplanar Tl-weighted and T2-weighted sequences. Coronal slices are particularly important in severe scoliosis. - CT:Three-dimensional reconstructions can be obtained for preoperative planning. ~ General

Radiographic signs of butterfly vertebra: Viewed in the coronal plane, the two halves of the vertebra taper toward the unfused center to produce a shape resembling a butterfly. Radiographic signs of lateral hemivertebra: Viewed in the coronal plane, one half of the vertebra tapers toward the center while the other half is absent, producing a nearly triangular or wedge shape. Radiographic signs of fused vertebrae: The A-P diameter of the fused vertebrae is diminished. often in combination with narrowing in the area of the disk inter-

space, which is either absent or underdeveloped. Fused vertebrae are about as high as two normal vertebrae including the interspace. In 50% of cases, the facets joints are also fused. The spinous processes can be malformed or fused as well. Localization: C2-(3 > C5-C6 > T12-Ll > 1.4-1.5.

21

Vertebral Malformations Fig. 1.16

Conventional A-P radiograph

of the cervicothoracic

junction of an

n.

11-year-old boy. Left hemivertebra at asymmetrical cervical vertebrae from T2 to the occiput. and complex segmenta-

tion and fusion anomalies.

Fig. 1.17 Conventional radiograph of the

lumbar spine (A-P.detail) of a 20-year-old patient. Incidental finding of a butterfly vertebra (arrow); additional findings include residual contrast agent projected on the adjacent caudal vertebra. which is also visualized.

22

Vertebral Malformations fig. 1.18a-c Schematic diagram of vertebral malformations (coronal view). Normal vertebra (a): lateral hemivertebra (b): butterfly vertebra (c).

a

Duu'- . u u

D

________ ~

-

71

-

c fig. 1.19 A 25-year-old woman with limited mobility in the cervical spine and

congenital vertebral fusion at (2-(3. Conventional lateral radiograph of the cervical spine.

23

Vertebral Malformations

G' ~

Fig.I.20 A 39-year-old man with vertebral fusion at (5-(6 in status post spon-

~

dylitis.Conventional lateral radiograph of

;:;-

the cervical spine.

s..

;;: Q

~

..•o'3 Q

"'"

~ Radiographic findings Primary imaging study to identify and determine the level of vertebral malformations • May be used to evaluate associated scoliosis where indicated. Typical butterfly, wedge. and fusion deformities are well visualized. Examiner can determine whether the abnormal vertebrae are supernumerary or have replaced normal

vertebrae.

~ CTfindings Axial slices are obtained to evaluate dysraphism of the posterior structures and vertebral evaluating

fusion anomalies. cleft vertebrae

Coronal

and sagittal

and hemivertebrae.

reconstructions

are useful for

and for preoperative

planning.

~ MRI findings Detection and evaluation of lipomas, diastematomyelia. or spinal cord compression • Evaluation ofthe spinal cord and exiting nerve roots. Clinical Aspects

............................................................................................

~ Typical presentation Usually asymptomatic • Often detected on radiographs obtained to evaluate scoliosis • Fused vertebrae may be associated with early osteochondrosis,

especially

in the caudally adjacent segments. Spinal stenosis is rarely encountered. ~ Therapeutic options Conservative treatment. Surgery (resection and/or fusion) is indicated only for

severe cases.

24

Vertebral Malformations

~;lf.~~~.~~~~~ .C?!?~~~~!~ Clefr verrebrae and hemiverrebrae

- Fracture: Usually rhere is a history of trauma. Two pedicles each per vertebra. Presence of an irregular fracture line lacking a cortical boundary. Associated soft tissue edema often present.

Congenirally fused

-

Isolated anomaly Klippel-Feil syndrome Basal cell nevus syndrome (Gorlin syndrome) Fibrodysplasia ossificans progressiva

-

Spinal fusion Posttraumatic Ankylosing spondylitis Post bacterial spondylitis Severe osteochondrosis Juvenile rheumatoid arthriris Alcoholic feropathy

vertebrae

Acquired verrebral fusion anomalies (no verrebral "waisr" heighr of offecred verrebra ofren reduced. especially onreriorly)

Selected

.

n o

" "[


s: Q ~ .., 3 Q

~

o' '""

References

Brossmann J. Czerny Ch. Freyschmidt J. Grenzen des Normalen und Anf.1nge des Pathologischen in der Radiologie des kindlichen und erwachsenen Skeletts. Stuttgart: Thieme 2001 Tortori-Donati P. Fondelli MP. Rossi A. Raybaud CA, eama A. Capra V. Segmental spinal dysgenesis: neuroradiologic findings with clinical and embryologic correlation. Am J Neuroradiol1999: 20: 445-456

25

Definition • Epidemiology Sporadic occurrence. 1 in 42 000 births. Familial genetic component. Females are affected slightly more often than males. Age range: Usually 10-30 years. • Etiology, pathophysiology, pathogenesis Congenital malformation of the cervical spine with failed segmentation of two or more vertebrae. Predilection: C2-0 > CS-C6 > craniocervical and thoracolumbar junctions.

Imoging Signs

............................................................................................

• Modality of choice Conventional radiographs: - Stress radiographs in maximum

flexion and extension are important

for eval-

uating instability. MRI: - To exclude spinal cord or nelVe root compression.

Abdominal ultrasound or CT: - To determine whether abdominal organs are affected. • General Vertebral fusion involving one or more segments with a narrow, rudimentary disk interspace. Often the facet joints and spinous processes are also fused. The vertebral body exhibits a shallowly concave "waist" at the level of the fused disk interspace. • Radiographic findings Visualization of typical cervical vertebral stenosis • Findings on stress radiographs: Lack of mobility in the affected segment, often with compensatory hypermobility in adjacent segments. Degenerative changes are often present in the adjacent segments. There may be a bony connection with the shoulder (extending from the scapula to the spinous process, vertebral arch, or transverse process of one or more lower cervical vertebrae).

• Cffindings Evaluation of the width of the spinal canal (stenosis due to degenerative changes in the adjacent segments or widening of the spinal canal in the presence of syringomyelia). • MRI findings Evaluation for possible disk protrusion. spinal or nerve root compression, and presence of Chiari I syndrome.

26

Klippel-Feil Syndrome Fig.

1.21 A 22-year-old woman with

limited mobility in the cervical spine and chronic pain radiating from the cervical spine. Clinical findings included short neck. Conventional lateral radiograph of

the cervical spine (detail). Synostosis at (5-(6

with rudimentary

anterior disk in-

terspace, narrowing of the fused (5-(6 vertebrae ("waist"), early degenerative changes in the adjacent segments (especially (4-(5).

Clinical Aspects • Typical presentatian Triad: - Short neck. - low posterior hairline.

- Limited mobility in the cervical spine. Some patients are asymptomatic whereas others show neurologic symptoms as infants and children. After age 3D,symptoms arise due to degenerative changes and instability in the adjacent spinal segments.

Often associated with other

anomalies (Sprengel deformity or elevated scapula, cervical ribs. pterygium colli. spina bifida, cleft palate. etc.). • Therapeutic aptians Initial conservative therapy. Surgery (spinal fusion) is indicated for severe pain despite conservative therapy and with increasing instability.

27

Differential Diagnosis ............................................................................................

s: Q

juvenile rheumatoid arthritis

- Inflammatory manifestations at other sites also - History

Post diskitis

- History - No "waist" - Irregular endplates

~

3

..•is'

Anky/osing

'"

Surgical spinal fusion

Q

spondylitis

:J

Selected

are usually present

- Typical. usually continuous. syndesmophytes - Symmetric involvement in the sacroiliac joints - History - No "waist"

References

Baba H, Maezawa Y, Furusawa N, Chen Q, Imura S.Tomita K.The cervical spine in the Klippel-Feil syndrome. A report of 57 cases. Int Orthop 1995: 19: 204-208 Guille JT. Miller A. 80wen JR. Forlin E. Caro PA. The natural history of Klippel-Feil syndrome: clinical. roentgenographic. and magnetic resonance imaging findings at adulthood. J Pediatr Orthop 1995; 15: 617-626 Reiser M. Peters PE. Radiologisehe Differenzialdiagnose der Skeletterkrankungen. Stuttgart: Thieme 1995

28

Definition ............................................................................................ Posteriorly convex curvature of the spine. The normal thoracic kyphosis develops naturally by 6 years of age as the child begins to walk upright. When the curvature exceeds the range of normal kyphosis (25-45°) it is considered abnormal kyphosis. _ Arcuate kyphasis (lang arc): In Scheuermann disease. ankylosing spondylitis, senile kyphosis. and postural deficiency. _ Angular kyphasis (shart arc): In spondylitis, compression fractures, pathologic fractures, tumors. and congenital wedge vertebrae.

Imaging Signs ............................................................................................ • Modality of choice Conventional radiographs. • Radiographic findings A lateral view with the patient standing helps determine the extent of deformity.

Lateral view in hyperextension

is taken to evaluate

nexibility

• Measure-

ment is similar to the Cobb method used for scoliosis; the distance measured extends from the superior end plate of the third thoracic vertebra to the inferior end plate of the twelfth thoracic vertebra. • CTand MRI findings These can be very useful for identifying the cause of kyphosis.

Clinical Aspects ............................................................................................ • Typical presentation Asymptomatic.

Functional

impairments.

Obstructed

vision.

Pain due to in-

creased degenerative changes. Neurologic deficits . •.. Therapeutic options Conservative treatment (corset, physical therapy, pain therapy) • Surgical management (correction. spinal fusion).

Differential Diagnosis ............................................................................................ Pastural kyphosis

Congenital kyphosis

- Note Schmorl nodes, Edgren-Vaino sign, Knutsson sign. - Note vertebral malformations such as

Neuromuscular kyphosis

- Palsies. ete.

Scheuermann disease

posterior

hemivertebrae

Myelomeningocele Pasttraumatic kyphosis

- History

latragenic kyphasis

- Post laminectomy.

excision of vertebra

- Post radiation therapy

29

Kyphosis Fig. 1.22 A 74-year-old man with known ankylosing spondylitis and increasing gibbus. post vertebroplasty. Conventionallateral radiograph of the thoracic spine of T9. Calcification of the longitudinal ligaments. slightly barrel-shaped vertebral bodies and abnormally increased thoracic kyphosis.

Fig. 1.23 A 74-year-old woman with gibbus and known osteoporosis. Conventionallateral radiograph of the thoracic spine. Vertebral height in the mid-thoracic spine is reduced especially anteriorly. leading to abnormally increased thoracic kyphosis. ·osteoporotic kyphosis.·

30

Kyphosis

Fig. 1.240, b

An 83-year-old

woman with gibbus. Conventional

of the thoracic spine (detail). Diffusely osteopenic

lateral radiograph

rarefied bone structure with multiple

vertebrae significantly reduced in height and showing marked degenerative changes. leading to abnormally increased thoracic kyphosis (a). Section of specimen showing corresponding changes (flattened and fishlike vertebrae) (b).

Kyphosis due to metabalic disease

- Osteoporosis - Osteogenesis imperfecta - Collapse of individual vertebrae

Kyphosis in skeleral dysplasia

- See vertebral

Kyphosis in ankylosing spondyliris

- Involvement

Collagen disorders

- Patient history

Kyphosis due ra rumor

- Often secondary

Kyphosis with inflammatory disorders

- Spondylitis

calcification

malformations of sacroiliac joints.

of paravertebral

ligaments

blastoma

Idiopathic kyphosis Senile kyphosis

- Significant narrowing of the disk interspaces with sclerosis along the adjacent end plates and later ankylosis; multiple vertebrae significantly reduced in height. typically with a flattened shape

31

Fig. 1.250, b A 60-year-old woman with known osteoporosis presented for follow-up radiograph (after 1 year) with bronchial asthma. Conventional lateral chest radiograph. Abnormal kyphosis of the thoracic spine with osteoporotic vertebral collapse in the midthoracic spine. "osteoporotic kyphosis."

Selected

References

Jager M. Wirth Cj. Praxis der Orthopadie. Stuttgart: Thieme 1986 Kormano M. Burgener FA. Radiologische Differentialdiagnostik matologie. Stuttgart: Thieme 1995

32

in Orthopadie

und Rheu-

Definition ............................................................................................ ~ Epidemiology Most common spinal disorder in adolescents (10% of the population); usually occurs at 10-18 years. Increased familial incidence. ~ Etiology, pathophysiology, pathogenesis Structural and growth disturbance of the vertebral end plates and disk margins leads to abnormal kyphosis in adolescence. Caused by chronic repetitive trauma to immature bone.

Imaging Signs ............................................................................................ ~ Modality of choice Conventional radiographs (supplemented by MRI when disk protrusion is suspected) . ••. General Reduction in disk height (more pronounced anteriorly) • Three or more thoracic vertebrae with barrel-like convex anterior margins (Knutsson sign) and/or a wedge shape. Later: Schmorl nodes (= chondroid disk defects in the region of the vertebral endplates) • Edgren-Vaino sign (exostoses on the endplate of the adjacent vertebra. opposite the cartilaginous nodules) • Separation of marginal ridges from the vertebral body and increased thoracic kyphosis (> 40°) • Sequelae characterized by degeneration and fusion of the anterior portions of the vertebrae can occur. 15% of patients also have scoliosis. Location: Usually in the thoracic spine and thoracolumbar junction, < 5% in the lumbar spine. very rarely in the cervical spine. ~ Radiographic findings Detects the signs described above. Used to measure the kyphosis. ~ CTfindings Better visualization of the changes in the vertebral endplates. ~ MRI findings Visualization of the frequently associated degenerative changes in the affected disks (disk narrowing. T2 signal loss. possible protrusion) • Schmorl nodes are hypointense on Tl-weighted images. hypointense or hyperintense on T2weighted images. Bone marrow edema may be present around the lesion . .... Nuclear medicine Bone scan may be normal or there may be increased focal uptake.

33

Scheuermann Disease fig. 1.26 Conventional lateral radiograph of the thoracic spine (detail) of a 20-year-old man with gibbus and back pain. Abnormal kyphosis of the thoracic spine with anteriorly reduced vertebral height. The anterior margins of the vertebrae are irregular: Scheuermann disease.

Fig. 1.27

Conventional lateral radiograph of the thoracic spine (detail) of an 18-year-old man with recurring back symptoms. Depression with sclerotic margins in the anterior portion of the

superior endplate of vertebra L2 (arrow; Schmorl nodules); there is a corresponding circumscribed bony projection in the inferior endplate of vertebra ll: Scheuermann disease.

34

Scheuermann Disease Clinical Aspects • Typical presentation Typical clinical presentation (thoracic kyphosis) • Increasing pain in the thoracic spine with exercise. Neurologic symptoms (kyphosis. disk protrusion) are rare . • Therapeutic options Conservative treatment and regular follow-up until 25 years of age (for kyphosis < 50· in an immature skeleton) • Corset (for kyphosis < 70· in an immature skeleton) • Surgery (spinal fusion; for kyphosis> 75· in an immature skeleton or > 60· in a mature skeleton. with severe uncontrollable pain or neurologic deficit).

Differential Diagnosis ............................................................................................ Postural kyphosis

- Normal vertebral end plates. returns to normal when

Congenital kyphosis Compressionfracture Tuberculous kyphosis

- Additional

spine is extended vertebral

abnormalities

are present

- Fracture line. bone marrow edema

- Extensive destruction of the vertebral endplates. soft tissue and bone marrow edema, and occasionally

fused vertebrae Kyphosis in osteogenesis imperfecta torda Ankylasing spandylitis Cartilaginous nodules on the vertebral endplates

- Vertebra plana. severe osteopenia

- Pathology in the sacroiliac joints - In the anterior half of the vertebra in Scheuermann disease

- In the posterior half of the vertebra in impaired regression of the notochord Selected References Ali RM. Green DW. Patel

Te.

Scheuermann's Kyphosis. CUff Opin Pediatr 1999: 11: 70-75

Tribus CB. Scheuermann's Kyphosis in adolescents and adults: diagnosis and management. JAm AcadOrthop Surg 1998; 6; 36-43 Wenger DR.FrickSL Scheuermann kyphosis.Spine 1999; 4; 2630-2639

35

~~~~!~~~~

.

• Epidemiology Occurs in 2-4% of the population. Females are affected about five times as often as males. Most often diagnosed in childhood or adolescence. • Etiology, pathophysiology, pathogenesis Scoliosis is defined as an abnormal lateral curvature of the spine. Classification according CO plane of curvature: - Right or left scoliosis (lateral deviation in the coronal plane). - Rotoscoliosis (rotation in the axial plane). - Kyphoscoliosis and lordoscoliosis (kyphotic and lordotic components in the sagittal plane). Classification by shape: - S-shaped scoliosis (double deviation with curve and reverse curve). - C-shaped scoliosis (single curve without reverse curve). End vertebrae: The most proximal and distal vertebrae of a curve. The vertebra at which the curve changes direction to become the reverse curve.

The vertebra

with the greatest tilt coward the concavity and usually the one least rotated. Neutra/ vertebra: The vertebra in a curve which exhibits no rotation (its alignment often matches that of the end vertebra). Apical vertebra: The vertebra in a curve which is furthest from normal position and exhibits the greatest rotation. Structural curve: Remains present in lateral bending views. Morphologic vertebral changes are seen (wedge vertebra. rotation). Nonstructural (functional) curve: Usually only slight. not progressive, and disappears completely with ipsilateral bending. Primary curve: Largest structural curve. Secondary curve: lesser curve. Compensacory curve: Curve located above or below the main curve. Imaging

Signs

............................................................................................

• Modality of choice Conventional radiographs. CT studies with coronal. sagittal. and possibly three-dimensional reconstructions may prove helpful in preoperative planning. Supplementary MRIstudies may be obtained when bone and spinal cord pathology is suspected (coronal and sagittal Tl-weighted and T2-weighted slices. and also axial T2-weighted slices at the level of the suspected pathology). • Radiographic findings A-P view with the patient standing (from occiput to sacrum) to measure the severity of scoliosis. Lateral view with the patient standing to evaluate additional abnotmal curves in the sagittal plane (required during initial examination as well as preoperatively and postoperatively) • Preoperative lateral bending views differentiate between structural and nonstructural curves. Cobb method of scoliosis measurement. The Cobb angle is determined as follows: Draw a line in the 36

Scoliosis

Fig.l.28 A 61-year-old man with chronic lower back pain. Conventional A-P radiograph of the lumbar and lower thoracic spine: Severe multisegmental degenerative changes (narrowed disk inters paces. subchondral sclerosis. osteophytes) with right convex scoliosis.

Fig.l.29 A 16-year-old girl with S-shaped scoliosis. Conventional A-P radiograph obtained with patient standing (overlaid

with grid).

37

Fig. 1.30 Schematic diagram of coronal view of S-shaped scoliosis showing left and right scoliosis.the Cobb angle (c), end vertebrae (E),apical vertebra (S).

plane of the proximal endplate of the cranial end vertebra and perpendicular to its longitudinal axis, and another similar line in the plane of the distal endplate of the caudal end vertebra, and then measure the angle where these two lines intersect. Follow-up studies are usually indicated at intervals of about 4-6 months (be alert to the radiation dose). • Cffindings Demonstrates complex congenital bony anomalies. Can exclude tumors. infectious pathology, and postoperative complications. • MRI findings To detect bone and spinal cord anomalies and exclude tumors and infectious pathology. Useful especially for atypical idiopathic scoliosis (left convex thoracic curve) and congenital scoliosis.

Clinical Aspects

............................................................................................

• Typical presentation Idiopathic scoliosis is usually asymptomatic. Painful scoliosis usually involves an abnormality. Degenerative disk changes are common. The rare cases of severe scoliosis may involve instability, neurologic symptoms, and breathing problems.

38

Scoliosis •.. Therapeutic options - For slightly abnormal curvature « 25°): Physical therapy. - For moderately abnormal curvature (25-50° in the thoracic spine or 25-40° in the lumbar spine): Corset and physical therapy. For severely abnormal curvature (> 50° in the thoracic spine or > 40° in the lumbar spine): Surgical management.

Differential Diagnosis Idiopathic

- Most common form, classic 5 curve, progresses with growth

Neuropathic

- Paralytic scoliosis in polio. meningomyelocele.

Myopathic

- In muscular

Congenital

- With vertebral

Merobolic

- Rickets, osteoporosis

and secondary to trauma or tumor, ere. dystrophy malformations

With tumor

- Painful curvature

Degenerative

- In adults. degenerative and facet joints

Compensorory

- With leg length difference:

Post spondylitis

- Painful curvature.

usually with short radius

Congenitol syndromes without vertebrol molformotions

- Neurofibromatosis. Marfan syndrome.

Ehlers-Danlos syndrome. osteogenesis imperfecta

Scheuermann disease

- Usually slight scoliosis

Selected

with short radius: MRI indicated changes

see

in the disks pelvis

References

Cassar-Pullicino VN. Eisenstein SM. Imaging in Scoliosis: What, Why and How? Clinical Radiology 2002: 57: 543-562 Greenspan A. Skelettradiologie. Munchen: Urban & Fischer 2002 Hedequist D. Emans J. Congenital scoliosis: a review and update. J Pediatr Orthop 2007; 27: 106-116

39

Definition ............................................................................................ Usually malrotation involves several spinal segments with simultaneous lateral curvature to the contralateral side. Rarely there is rotation of a single vertebra.

commonly associated with morphologic anomalies (especially asymmetry of the facet joints) • DDshould consider diskogenic. arthrogenous. and reflexive causes. Imoging Signs ............................................................................................ ~ Modality of choice Conventional radiographs. MRI may be carried out to evaluate whether the rotation also involves spinal stenosis, or if there is nerve root compression or a diskogenic cause. ~ Radiographic findings An A-P view is obtained to evaluate whether the rotation is multisegmental or involves only a single vertebra. and to determine the extent of vertebral rotation • Vertebral rotation can be measured by determining the position of the pedicles or spinous process relative to the imaginary midline of the vertebra or relative to the lateral contours of the vertebra. These methods of measurement are usually not suitable for determining whether rotation has increased. Signs ofrototion: The rotated vertebra is tilted toward the contralateral side. The spinous process shifts toward the contralateral side. The contralateral pedicle may be projected outside the lateral margin of the vertebra whereas the ipsilateral pedicle is projected within the vertebra. The facet joint on the contralateral side is narrowed. and widened on the ipsilateral side. The facet joint spaces are projected on the vertebra to the side opposite the direction of rotation. ~ CTfindings The degree of rotation with respect to the adjacent vertebrae can be measured. ~ MRI findings The width of the spinal canal. disk. and nerve roots can be measured. Clinicol Aspects ~ Typical presentation May be asymptomatic or involve localized or radiating pain. ~ Therapeutic options Depending on the cause and severity of symptoms. treatment is conservative or

surgical (for example with severe scoliosis).

40

Malrotation

Fig. 1.31

A 39-year-old man with low back pain. Conventional A-P radiograph of the lumbar spine. Partial sacralization of the L5 vertebra with right pseudarthrosis. The spinous process of vertebra L4 (and to a lesser extent that of L3) is shifted slightly to the right. Findings suggest slight leftward rotation of vertebrae L3 and L4 due to partial fusion of a transitional vertebra.

A 45-year-old man with low back pain. Conventional A-P radiograph of the iumbar spine. Slight left (onvex (urve in the lumbar spine. The spinous processes of vertebrae L3, L4, and L5 are shifted slightly to the right. Findings suggest slight leftward rotation of vertebrae l3. L4, and L5 combined with slight left convex scoliosis. Fig.1.32

41

Malrotation Fig. 1.330-c

Schematic diagram of coronal view of vertebral rotation. la evaluate rotation, note the distance between the spinous process and the lateral outer contour

a

of the vertebral

body. Where distance X equals distance Y. there is no rotation (a). Where distance X is not equal to distance Y, rotation is present (b. c).

b

c

Differential Diagnosis ............................................................................................ Trauma

Rotation with scoliosis Rotation with specific morphologic anomalies Rotation with blockage due to diskagenic, arthrogenous, or reflexive causes

- Facet joint asymmetry

Selected References Gutmann G, Biedermann H. Funktionelle gart: Gustav Fischer 1992

Pathologie

und Klinik der WirbelsauJe.

Stutt-

Nash CLjr, MoejH. A study of vertebral rotation.j Bonejoint Surg Am 1969: 51: 223-229

42

:;<

General

Q

r::

The severity of the injury increases from type A to type C.as it does within the subdivisions of each specific type of fracture. Type A and type B injuries are often occur together. Today. the Magerl classification is preferred to the Denis three-column classification.

The Magerl classification

3 Q

structure provides a more precise in-

dication of the degree of instability/stability of the fracture than previous classifications

• Only compression

fractures

without

involvement

of the posterior

margin

are definitively classified as stable. Involvement of the posterior margin is often poorly visualized on conventional plain films. Generous criteria should be applied when determining whether IT is indicated. Type A ............................................................................................ •.. Mechanism

Compression.

• Radiologic characteristics Reduced height of vertebra. Fissured vertebra. tance • Intraspinal fragments.

Increased interpedicular dis-

TypeB

............................................................................................ •.. Mechanism Distraction.

• Radiologic characteristics Distance between spinous processes increased. Subluxation or dislocation of the facet joints. Abnormally high posterior vertebral margin. Transverse fractures • Fragments avulsed from the posterior corners of the vertebral body. TypeC

............................................................................................ •.. Mechanism

Rotation.

• Radiologic characteristics Vertebrae laterally displaced. displaced.

Asymmetry of the pedicles • Spinous processes

Fractures of the transverse

processes.

Unilateral

cation. and/or fracture of posterior partS of the vertebra.

subluxation.

dislo-

Unilateral rib fracture

or dislocation.

Selected References Magerl F. Aebi M. Gertzbein

SO. Harms

J.

Nazarian S. A comprehensive

classification or

thoracic and lumbar injuries. EurSpine J 1994:3: 184-201

43

Spinallnjury-Magerl :;t Q c:

Classification

Al

81

A2

82

A3

83

(1

3 Q

F;g.1.1 to 1.3 Type A: Al-Impaction

C2

C3

fractures, stable. A2-C1eavage fractures, usually stable.

A3-Burst fractures. stability varies. Type D: 81-Posterior ligament tear with disk involvement and associated type A injury. B2-Posterior bony ligament avulsion with fracture of the vertebral body or interverte· bral disk or associated type A injury. B3-Torn

intervertebral

disk with subluxation

or fracture of the articular processes. with spondylolysis or posterior dislocation. All type B injuries are unstable. Type C: Cl-Type A injury with rotation. C2-Type B injury with rotation. O-Rotational shear fractures. All fractures in group C are highly unstable.

44

Definition ............................................................................................ •

Epidemiology The annual incidence of vertebral Fractures in women over 70 years of age is 2 J %: aFter 80 years it is 50% • Women are aFFected twice as oFten as men. • Etiology, pathophysiology, pathogenesis Symptoms range From circumscribed upper back pain to distal neurologic defi-

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cits. Traumatic: High-energy trauma produces a Fracture in previously healthy bone. Osteaparotic: Slight trauma or everyday activity produces a Fracture in weak. osteoporotic bone. Typical sites include the middle and lower thoracic or upper lumbar spine. Fishlike or wedge-shaped vertebrae. Vertebral collapse also occurs elsewhere in the spine • Intravertebral gas phenomenon. Findings include radiodense bands in the endplates (callus Formation) • Osteopenic bone structure. Malignant: Even normal exercise or slight trauma causes a fracture of the vertebra. whose stability is compromised by a primary or secondary malignant process, such as metastasis or multiple myeloma. Pathalogicfracture: Fracture From normally inadequate loading. Insufficiency fracture: Fracture with abnormal bone structure.

Imaging Signs-Osteoporotic Fracture ............................................................................................ •

Modality of choice Conventional A-P and lateral radiographs. MRI (OWl where indicated). • Radiographic findings Typical sites include the middle and lower thoracic or upper lumbar spine. Fishlike or wedge-shaped vertebrae. Vertebral collapse also occurs elsewhere in the spine. Intravertebral gas phenomenon. Findings include radiodense bands in the endplates (callus Formation) • Osteopenic bone structure. •

MRI findings DiFFuse bone marrow edema in an acute Fracture. Occasionally there is a halolike paravertebral soFt tissue edema. Fluid sign. Gas phenomenon in the vertebral body or in the regions of the Facet joints. Edematous changes recede and are increasingly converted to Fatty marrow. Elevated diFFusion coefficient.

Imaging Signs-Malignant

Frocture ............................................................................................ •

Modality of choice Conventional A-P and lateral radiographs. MRI (OWl where indicated). • Radiographic findings Inhomogeneous vertebral density is a sign of metastatic involvement. Vertebral arches are also aFFected. Atypical localization. (solitary Fractures above T7 in particular are suspicious) • Often there is a unilateral reduction in height on the A-P film.

4S

VertebralFractures~auses ::;4 Q

Osteoporosis

:3

Band of hypointensity (Tl) or hyperintensity

c: Q

Osteoporosis Complete hypointensity (Tl ) or hyperintensity

(T2, STIR)

Metastasis Tumor and edema extend into the paravertebral soft tissue

(T2,STIR)

N

[q;\ !c$;?'' '. Inhomogeneous edema Fig.2.4

Distinguishing

Arch almost invariably spared osteoporotic

Homogeneous edema

vertebral fradures

from metastatic

fractures on

MRI.

Fig.2.50-c Conventional radiographs (a). Osteoporotic compression fracture with vertebral wedge deformity. MR image (sagittal, STIR)(b). Acute vertebral collapse with significant edema. Follow-up radiograph after kyphectomy (c).

• CTfindings •

Focal or epidural soft tissue mass. MRI findings Solid enhancing mass extending past the margins of the vertebra.

Compression

of the vertebra pushes the tumor into the paravertebral soft tissue. creating a 46

Vertebral Fractures-Causes convex bulge in the posterior margin of the vertebra. The tumor is often distinguishable from the surrounding edema. Often asymmetric. Reduced diffusion coefficient.

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3 c

Clinical Aspects

............................................................................................ • Typical presentation Clinical symptoms are highly variable. Stable fractures can be asymptomatic. Osteoporotic fractures lead to increasing thoracic kyphosis.

""Complications Severe neurologic symptoms including paraplegia can occur. depending on the site of injury. • What does the clinician want to know? Acute or chronic fracture? • Stable or unstable? • Osteoporotic or metastatic? • Which imaging modality should be used? Differentiating law-risk and high-risk-patients (Canadian nexus study): Radiologic examination is indicated in patients with: - Abnormal alertness. - Intoxication. - Neurologic deficit. - Bleeding in the brain. - Painful dorsal midline. - Distraction injury. - Multiple fractures continuation. Low-risk patients should fulfill all three low-risk criteria: - No high-risk factor (age> 50 years. high-risk trauma. paresthesia of extremities). - Presence of low-risk factors (minor car crash. sitting position. no pain in dorsal midline). - Active skull rotation> 45" is possible 011 both sides. High-risk patients are those who: - Have experienced high-energy trauma (velocity> 50 kmfh: fall from a height of more than 3 m) - Are> 50 years of age. - Are unconsciousness. High-risk patients need a spiral CT exam! • Therapeutic options Treatment depends on the neurologic symptoms and the severity of injury • Conservative therapy is indicated for stable fractures without neurologic symptoms· In all other cases. surgical management with appropriate stabilization of the spine is indicated. Alternatives include kyphectomy or vertebroplasty. Selected References Baur A.. Dietrich

0 .. Reiser M. Diffusion-weighted

imaging

of bone marrow:

current

sta-

tus. Eur Radiol. 2003: 13: 1699-1708 Daffner RH. Radiologische Diagnostik der Wirbelsaule. Stuttgart: Thieme 2003

47

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Definition ............................................................................................ ~ Epidemiology Fractures of the dens account for 11-13% of all cervical spine injuries (in children up to 75%) • The most often diagnosed injury in the upper cervical spine. ~ Etiology, pathophysiology, pathogenesis Caused by hyperextension, extreme nexion, or even lateral bending' Osteoporosis predisposes to type II fractures and subsequent nonunion of the fragments. Fracture types according to the Anderson and d'Alonzo classification: - Type I (8%): Oblique fracture through the superior tip of the dens with avulsion of the alar ligament-stable. - Type II(59%): Fracture at the base of the dens-unstable. - Type III (33%): The fracture extends into the axis body (actually a C2 fracture) and may be stable or unstable (horizontal fractures in the upper third are more stable than oblique fractures coursing anteriorly in the middle or lower third). Imoging Signs ............................................................................................ ~ Modality of choice Multislice spiral CT(where a dens fracture is suspected). MRI(where spinal cord or vascular injury is suspected). ~ Radiographic findings Direct visualization

of the fracture line.

Demonstrates

indirect signs such as

displacement of the dens, especially posteriorly' Prevertebral soft tissue swelling is often the only sign of a dens fracture (relatively specific, not very sensitive). ~ CTfindings Axial multislice CTwith thin slices (I mm) • Reconstruction in a high-resolution bone window with sagittal and coronal slices. Fracture line. Degree of displacement . • MRI findings Tl-weighted (sagittal. coronal): - Visualization of the fracture and degree of displacement. Integrity of the ligaments (especially the alar ligaments). Tl-weighted, STIR(sagittal): - Visualization of the bone marrow and soft tissue edema and/or injuries to the surrounding soft tissue.

This distinguishes acute injury from chronic non-

union. MRIcan also visualize pathology in the spinal cord (impinging edema. necrosis. bleeding, severed spinal cord) • Avulsion of the vertebral artery.

48

Dens Fracture

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Fig. 2.60, b Dens fracture. Schematic diagram (a) of the Anderson and d'Alonzo classification: types I, II, and 111.Conventional lateral radiograph (b). Dens fracture with severe anterior displacement.

Fig. 2.7a. b CTof (1-(2 (a coronal and b sagittal reconstructions): fracture (Anderson and d'Alonzo type II).

Displaced dens

49

Dens Fracture

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c:

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Clinical Aspects

............................................................................................

~ Typical presentation Neck pain' Neurologic symptoms are rare. cial, or other injuries.

41 % of patients also have head. faMost patients cannot sit up from a supine position with-

out using their hands. ~ Complications Compression of the vertebral artery with brainstem symptoms: very rarely spinal cord injuries from displaced comminuted fractures. ~ Therapeutic options - Type I: Four weeks of immobilization. - Type 1/: Where the injury is unstable. primary fusion is indicated to avoid myelopathy. - Type 11/: Stable injuries are immobilized with a halo brace and later a corset. Unstable injuries require surgical fixation. Differential

Diagnosis

............................................................................................

Physiologic fusion at age 11-12 Os odontoideum

Subdural synostosis Subluxation in rheumatoid arthritis Pseudarthrosis secondary to chronic fracture

- Failure of congenital fusion of the tip of the dens - No soft tissue swelling. typical round to oval configuration. smooth cortex - No history of trauma. absence of clinical signs - May persist until adolescence - Dens is destroyed by an arthritic process. leading to subluxation and possible instability - History - Sclerotic halo

Selected References Burke]T.HarrisjH. Acute injuries ofche axis vertebra. Skel Radio11989: 18: 335-446 Silberstein M. Hennessy O. Prevertebral swelling in cervical spine injury: identification of

ligament injury with MRI.ClinicalRadiology1992: 46: 318-323

50

Definition ............................................................................................ • Epidemiology Accounts for approximately 46% of cervical spine injuries. • Etiology, pathophysiology, pathogenesis Results from maximum flexion of the cervical spine. Maximum extension of posterior vertebral elements and compression of anterior elements. ciated with anterior disk herniation.

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Often asso-

The most important types of flexion fracture are: Anterior wedge fracture: Least severe form of flexion injuty • Avulsion of a fragment from the anterior margin of the superior end plate with an intact posterior margin. Higher energy trauma will produce a wedge vertebra and may involve the posterior margin.

Teardrop fracture: A triangular fragment resembling a teardrop is avulsed from the anteroinferior aspect of the vertebral body in flexion. This is usually combined with a tear in the posterior longitudinal ligament • Although the posterior margin is not affected, the injuty is unstable. Often a cause of paraplegia. Occurs in the lower cervical spine (C5) in 70% of cases. Anterior subluxation or dislocation: Tearing of the posterior ligament complex or avulsion of the ligament from the vertebral body causes one vertebra within a segment to tilt anteriorly relative to the adjacent caudal vertebra. Stability depends on the severity of the angulation and translation. Imoging Signs ............................................................................................ • Modality of choice Multislice CT - Slice thickness in the cervical spine 1 mm to maximum 3 mm with sagittal reconstructions.

- Where spinal cord injuries or injuries to the ligament complex are suspected. MRI.

• Radiographic findings Compression of the vertebral body. Disrupted alignment. Prevertebral softlissue swelling (normal appearance of soft tissue does not exclude a fracture) • Avulsion of the anterior margin of the superior end plate in an anterior wedge fracture. Avulsion of the anterior margin of the inferior end plate in a teardrop fracture. In anterior subluxation ordislocation, one vertebral body is tilted anteriorly. opening a gap between the spinous processes and causing incomplete ar-

ticulation ofthe facet joints. The subluxed vertebra may be displaced anteriorly. • CTfindings The signs seen on conventional radiographs are also visualized on CT,although with far greater sensitivity. Sagittal reformations are helpful. • MRI findings Tl-weighted. T2-weighted STIR:The fracture and degree of displacement are visualized • Integrity ofthe ligament complex can be evaluated. Spinal cord edema and/or bleeding are visualized. 51

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a

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Fig. 2.80, b

Schematic diagram (a). Anterior wedge fracture with rupture of the poste· rior longitudinal ligament. spinal canal stenosis. and spinal cord compression. Conven· tionallateral radiograph of the cervical spine (b). Teardrop fracture with widening of the facet joint space.

Fig. 2.90, b CT of the cervical spine (a coronal and b sagittal, volume-rendered). Teardrop fracture of (6 with posterior displacement of the vertebral body. To better visualize the injury. the respective slices anterior to the imaging plane have been cut away.

52

Flexion Fracture of the Cervical Spine

Clinical Aspects .........................................................................•..................

3

- Typical presentation Trauma

consistent

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Q

Q

with

imaging

findings

• Severe

neck pain

• Neurologic

symptoms mayor may not be present. - Complications Spinal cord injuries

with distal neurologic

symptoms.

- Therapeutic options Depends on the neurologic symptoms and degree of injury. Halo fixator is indicated in the absence of neurologic symptoms. Immediate decompression is indicated where neurologic symptoms and spinal cord compression are present. Selected References BurkeJT.HarrisJH.Acute injuries afthe axis vertebra. Skel Radial 1989: 18: 335-446 Galanski M. Wippermann

B. Stamm G. Sazak N. Wafer A. Kompendium

der traurnatologi-

schen Ronrgendiagnostik. Berlin: Springer 1999

53

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3

Q

Definition ............................................................................................ • Epidemiology Rare. Account for only 1.5%of all spinal injuries. • Etiology, pathophysiology, pathogenesis Caused by impaction with purely axial compression (as in a jump from a great height) • Localized largely in the thoracolumbar region, although such injuries may also occur in the lower thoracic spine.

Neurologic symptoms occur where

fragments are displaced into the spinal canal. Unstable when the posterior margin of the vertebra is also involved. Compression fracture. Fracture types: Incomplete burstfracture: Fracture involving primarily the anterior margin of the superior end plate and underlying portion of the vertebral body. Burst/fissure fracture: Invariably bisegmental, burst zones in the vertebral body are combined with fissure fractures of the other areas of the body. Complete burstfracture: Complete destruction of the entire vertebral body. Loss of axial load-bearing capability. Imaging Signs ............................................................................................ • Modality of choice Multislice CT: Primary modality in severe multiple trauma. In other cases, conventional

radiographs

in two planes will suffice.

Where neurologic symptoms are present: Supplementary MRI. • Radiographic findings Vertebral height is reduced. A vertical and/or horizontal fracture line may be directly visualized. Increased interpedicular distance. In the cervical spine. the traumatized segment may show slight extension or kyphosis on the lateral

film. Partial or complete bulging of the posterior margin of the vertebra (often difficult to detect on a plain film). • Cffindings Axial multislice CT with thin slices (cervical spine: 1 mm: thoracic and lumbar spine: 3 mm) • Sagittal and coronal reconstructions in the soft tissue window and high-resolution window.

Images show the same signs as conventional ra-

diographs • The fracture line and the position of the posterior fragment relative to the spinal canal are better visualized. mas are visualized.

• MRI findings Sagittal and axial Tl-weighted where Cf fails to demonstrate tensity and height of vertebra tense on the STIRsequence.

Bone fragments and epidural hemato-

and T2-weighted STIRsequences. Indicated only a correlate for neurologic symptoms. Signal inare reduced on Tl images. Vertebra is hyperinPrevertebral hematoma. Blood in the spinal ca-

nal. Spinal cord contusion (edema and swelling).

54

Burst Fracture of the Spine :;t Q c:

3 Q

Fig. 2.100. b Schematic diagram of burst fracture (a). Conventional tomogram T12 (coronal; b). Vertical fracture line with bilateral lateral displacement. Impression fracture from the caudal vertebra.

Fig. 2.11o. b Conventional radiograph ofthe thoracolumbar junction (A-P.a). Complete burst fracture of vertebra L1. The height of the vertebral body is reduced and the interpedicular distance markedly widened. Conventional lateral radiograph (b). Significant reduction in anterior height with bulging of the posterior margin of the vertebra.

55

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3

, ..... ,',

,..- .

,

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Q

/.

. . .'.-

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Fig.2.120-c CT ofT12 (sagittal reconstruction) (a). Complete burst fracture with compression of the dural sac. CT (b coronal and c axial). Fracture of the inferior end plate and marked spinal

stenosis.

\

....

~.

l(

,

\.

,."

",'

"

\,

(

",

...

"

Burst Fracture

of the Spine :;<

Clinical Aspects

·.....................................................................................•.....

Q

l::

•. Typical presentation Highly variable depending on the severity of injury. History of trauma. Circumscribed back pain. Radiculopathy or myelopathy may be present. • Complications Variable neurologic deficits including paraplegia. • What does the clinician want to know? Relationship of vertebral fragments to spinal canal. Possible risks of secondary

3 Q

neurologic complications.

• Therapeutic options Conservative functional therapy for stable nondisplaced fractures • Surgical treatment for injuries with neurologic deficits. unstable injuries. and spinal fractures in ankylosing sion.

spondylitis.

Direct screw fixation of fragments.

Spinal fu-

Selected References Galanski

M. Wippermann

B. Stamm

G. Sazak N. Wafer A. Kompendium

der traumatologi-

schen Rontgendiagnostik. Berlin: Springer 1999 Kinzl L.Arand M. Fleischmann W. Trauma der Wirbelsaule. In Kinzl L.Traumatologie. 2nd ed. Munich: lomoschitz

Urban und 5chwarzenberg

F. Bildgebung

1993

bei Wirbelsaulenverletzungen

- Diagnostic

Imaging.

Wien

Med

Wochenschr 2001: 151:502-505

57

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Definition ~ Epidemiology Less common than burst or compression fractures.

~ Etiology, pathophysiology, pathogenesis Horizontal vertebral fracture and/or horizontal soft tissue laceration. especially at the thoracolumbar junction (T11-l3). Classic mechanism of injury (based on the Denis classification): Compression of the anterior column (anterior third of the vertebral body and anterior longitudinalligament) and distraction of the middle column (posterior third of the vertebral body and posterior longitudinal ligament) and posterior column (vertebral arches. facet joints, spinous process, and transverse process) as a result of anterior hyperflexion over the lap belt in a car. which acts as a fulcrum. Imoging Signs

............................................................................................

~ Modality of choice cr with sagittal and coronal reconstructions. Most reliable method of preoperative diagnosis and of differentiating a Chance fracture from a burst or compression fracture.

~ General The distance between

the spinous processes is increased or the spinous process-

es are fractured at the level of the main fracture. Often the fractured vertebra exhibits wedge deformation with a reduction in anterior height and secondary focal kyphosis. ~ Radiographic findings Usually the initial imaging study. Radiographs in at least two planes should be obtained. Supplementary stress radiographs or oblique views are obtained where indicated. ~ CTfindings For better evaluating the extent of the fracture, especially in the posterior column.

~ MRI findings For detecting discrete fractures (vertebral body edema and discrete fracture line) • For detecting ruptures of the longitudinal ligaments (the posterior longitudinalligament in particular is often affected) and the interspinous ligaments. For detecting spinal cord contusions. Clinicol Aspects

............................................................................................

~ Typical presentation Low back pain secondary to high-speed trauma. ~ Therapeutic options Surgical treatment is usually indicated.

58

Chance Fracture (Seat Belt Fracture) ::;l Q

c:

3 Q

Fig. 2.13 a. b A lO-year-old girl presented with pain in the lumbar spine after a traffic accident 2 days previously. Conventional radiographs of the lumbar spine (a lateral, b oblique). Radiolucent line coursing horizontally through the spinous process. lamina, and posterior body of the third lumbar vertebra. The line narrows from posterior to

anterior: Chance fracture of L3.

Differential Diagnosis Compression fracture

- Results from axial forces with or without nexion; posttraumatic. osteoporotic, or tumor related

Burst fracture

- Results from axial forces; vertical fracture. normal distance between spinous processes

Shear fracture

- Results from transverse forces: all three columns are discontinuous. olisthesis

Distraction injury

- Results from vertical distraction or hyperextension: all three columns are discontinuous. distraction and/or olisthesis

Selected References Ross)S, Brant-Zawadzki M, Moore KR.Diagnostic Imaging Spine. Salt Lake City: Amirsys 2004

59

:;4 Q

Definition ............................................................................................

3

•

l:: Q

Epidemiology

Cl fractures: Account for approximately 6%of all spinal fractures. •

Etiology, pathophysiology,

pathogenesis

Abnormal pressure of the occipital condyles on the atlas with the head extended.

Compression fracture.

Often occurs in combination with avulsion of the

transverse ligament of the atlas. Unstable. Burst fracture of the atlas. Classification of fractures of the atlas: Type 1: Fracture of the anterior arch of the atlas. Extension fracture. Usually stable. Often combined with a dens fracture. Type 2: Fracture of the posterior arch of the atlas. Typical extension fracture. The posterior arch of the atlas is compressed between the occiput and C2 and fractures. Stable fracture. Type 3: Jefferson fracture. Fracture of the anterior and posterior arches of the atlas. Imoging Signs •

Modality of choice

- Multislice CT:Primary modality in multiple trauma or where there is a strong suspicion of a fracture. Conventional radiographs of the cervical spine. - MRI: Primary modaliry when ligament instability is suspected. - Multislice CT is indicated where conventional radiographs are equivocal or suggest displacement of the lateral masses. •

Radiographic

findings

The fracture lines are directly visualized. Displacement of the lateral masses of the atlas. Offset in the lateral atlantoaxial joints. The lateral film may show anterior

•

soft tissue swelling.

CTfindings

Multislice CTwith slice thickness of 1-2 mm • Bone and soft tissue windows. Precisely demonstrates fracture, exact location of injury. and signs of complica•

tions. MRI findings

Axial and coronal T1- and T2-weighted STIRsequences. edema.

Visualization of acute

Visualization of ligament injuries.

Clinicol Aspects ............................................................................................ • Typical presentation

Pain in the upper cervical spine. • Complications

Simultaneous injuries to other cervical vertebrae are common. bility • Usually heals without

complications.

Ligament insta-

Recurrent displacement

with

widening of the C1 ring and posttraumatic degenerative joint disease can occasionally occur with purely conservative therapy. 60

jefferson Fracture Flg.2.14 Schematic diagram of atlas fractures.

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Flg.2.15 Schematic diagram of radiographic signs in atlas fractures.

lateralized lateral mass in (1

Difference> 5 mm -ligament

rupture

Fig. 2.16 a. b

Conventional A-P radiograph (aj. Severe cervical spine trauma. offset sign. Laterally displaced lateral masses. CT of C1-(2 (axial; b). Type 3 Jefferson fracture.

61

jefferson Fradure

~ Q c:

3 Q

• What does the clinician want to know? Is the injury stable or unstable? • Are other vertebrae involved? • Therapeutic options Types 1 and 2: Stable fractures. Immobilization in a neck collar for 4-6 weeks. Type 3: Usually immobilization with a halo brace for 10 weeks. Open reduction and internal fixation with plate and screws through an anterior or posterior approach may be indicated.

Differential Diagnosis Apparent spreading apart of the lateral masses Congenital variants

- Findings are easily confused in children up to 4 years of age - Jefferson fractures are rare in children - Failure of fusion of the vertebral arch or other normal variants or anomalies - Pseudo "fracture lines" are less sharply defined and/or sclerotic

Selected References Galanski M. Wippermann B. Stamm G. Sazak N. Wafer A. Kompendium der traumatologischen Rontgendiagnostik. Berlin: Springer 1999

Scharen S,Jeanneret B.Atlas fractures, Orthopade. 1999: 28: 385-393

62

Definition

............................................................................................ ~ Epidemiology Second most common injury to the cervical spine after the dens fracture (approximately 7%of injuries). ~ Etiology, pathophysiology, pathogenesis Nowadays usually caused by head-on vehicle collision in which the forehead strikes the dashboard or steering wheel, and is immediately followed by extreme extension of the upper cervical spine (deceleration trauma) • Extreme extension alone results from a rear-end collision with the vehicle behind. and without a headrest. A high bending moment acts on the weak connections of the neural arch of the axis. Traumatic spondylolisthesis of C2 • Isthmus fracture. Pedicle

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fracture.

Effendi classification: - Type 1: Bilateral nondisplaced arch fractures (potentially unstable). - Type 2: Diastasis in the arch with angulation between C2 and C3 > 10· (unstable). - Type 3: Distance between C2 and C3 exceeding 3.5 mm (unstable, complete disk tear and complete tears of the anterior and posterior longitudinal ligaments). Imaging Signs ............................................................................................ ~ Modality of choice - Spiral CT:Primary modality in multiple trauma or when there is strong clinical suspicion of a fracture. Conventional radiographs of the cervical spine. - MRI: Primary modality when ligament instability is suspected. - Spiral

cr

is indicated where conventional

radiographs are equivocal.

~ Radiographic findings The fracture plane courses obliquely from anteroinferior to posterosuperior.

This makes nondisplaced fractures difficult to detect.

Avulsed fragments from

the anteroinferior margin of (2 or the anterosuperior margin of (3 indicate a

tear in the anterior longitudinal ligament • Anterior slippage of C2 is a sign of instability from rupture of the fibrous connections between disk and ligament. "Fat C2 sign" (the inferior end plate of C2 appears elongated along the superior end plate of C3, an illusion created by a vertebral fragment remaining in situ as the rest of C2 displaces). ~ CTfindings Multislice CTwith slice thickness of 1-2 mm • Bone and soft tissue windows. Multiplanar reconstructions. Fractures are readily demonstrated, as is any displacement. which is a sign of rupture of the fibrous connections between disk and ligament. Soft tissue swelling anterior to C2. ~ MRI findings Tl- and T2-weighted STIRsagittal. axial. and coronal where indicated. Useful mainly for visualizing ligament injuries. Edema sign on the STIRT2 sequences • The T1 sequence may show the fracture. 63

Hangman's

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c:

Fracture

a

Q

Fig. 2.17a, b Schematic diagram of hangman's fracture (a). Conventional lateral radio· graph (b). Type I C2 fracture in a 7-year-old girl.

Rg.l.J8a.b

Conventional

lateral radiograph (a). Type III hangman's fracture. C2 is an-

teriorly displaced and the (2-0 fractured.

Posterior alignment

interspace is widened anteriorly. The C2 pedicles are is disrupted. The arch of the atlas is also fractured.

CT of C2 (axial, b). Hangman's fracture.

64

Hangman'5

Fracture

~Ii?f~~' ~p.~~~

.

• Typical presentation Appropriate history findings. Pain in the upper cervical spine region. Neurologic symptoms are rare (maximum of2S% of all cases) because the spinal canal is relatively wide in this region .

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... Complications Simultaneous injury to (lor injury to the vertebral artery. Undetected instability with late neurologic symptoms. Symptoms depend on neurologic damage. Secondary joint degeneration may occur. • What does the clinician want to know7 Is the injury stable or unstable7 • Therapeutic options Type I: Six weeks of immobilization in a neck collar. Type 2: Selected cases may be immobilized for six weeks in a halo brace. othet-

wise direct Judet screw fixation of the arch of the axis is indicated. Type 3: Anterior (or anteroposterior) graft and plate fixation.

fusion of C2-C3 with an interposed

bone

Differential Diagnosis · ...•....................................................................................... Pseudosubluxarian

Selected

_ Approximately 20% of all children up to 8 years of age show physiologic anterior slippage of C2 or even C3 - Alignment of the spinous processes and laminae is preserved - No soft tissue swelling

References

Effendi B. Ray D.Cornish B. Dussault RG.l.aurin CA. Fractures of the ring ofthe axis.J Bone Joint Surg 1981: 63 B: 319-327 Galanski

M. Wippermann

B. Stamm

G. Bazak N. Wafer

sehen Ronrgendiagnostik. Berlin: Springer 1999 Samaha C et .11.Hangman's fracture: the relationship

A. Kompendium between

asymmetry

der traumatologiand instability.

J Bone Joint 5urg IBr12000; 82: 1046-1052

65

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Definition ............................................................................................ • Epidemiology Damage to the spinal cord occurs in 10-30% of spinal injuries. In cervical spine trauma. purely 50ft tissue injuries without bony involvement predominate. Frequency of cervical spine injuries increases from cranial to caudal.

• Etiology, pathophysiology, pathogenesis Most cervical spine injuries involve ligament injuries and not bone or spinal

cord. They lead to a posttraumatic reflex sympathetic dystrophy syndrome. Primal)' spinal cord injuries are directly related to the trauma. Secondal)' damage results from edema. circulatol)' disturbances, or late-onset hemorrhage. Spinal shock is seen relatively often in young athletes. Spinal shock results from a reversible complete loss of conduction with characteristic symptoms. No synonyms. Classification: - Spinal shack spinal concussion = neurapraxia: Temporal)'. fully reversible loss of function in the spinal cord that may include complete cervical cord synz

drome or anterior or posterior cord syndrome with characteristic

symptoms.

depending on the site of injul)'. - Spinal contusion: Transient compression of the spinal cord. - Spinal cord compression: Persistent impingement. Imaging Signs ............................................................................................ • Modality of choice MRI should be the primal)' study when a spinal cord injul)' is suspected (Caution: Clinical and imaging signs may appear several days after trauma!). • Radiographic findings Not significant.

• CTfindings Spiral CTof the cervical spine with maximum slice thickness of 2 mm • Reconstruction in sagittal and axial planes. Demonstrates directly bony injuries to the cervical spine and the possible cause of spinal cord damage. May demonstrate disk displacement. • MRI findings Sagittal T1-, T2-weighted. STIRsequences. Axial T2 sequence in the affected segments. Precisely localization and visualization of spinal cord damage (edema. hemorrhage, disk displacement) • Demonstrates ligament injuries (edema sign on STIRan Tl-weighted images) • In spinal shock. the spinal cord will occasionally appear slightly swollen and slightly hyperintense over a short distance. In a contusion. findings include a swollen, clearly edematous spinal cord (hyperintense on STIRimages).

66

Spinal Cord Trauma ::;l

"3 t:

"

Fig. 2.190. b

MR images of the cervical spine (a) (sagittal.

Marked hyperintense

signal alteration

T2). Slight spinal cord edema.

at the base of the dens. Type II dens fracture

(b)

(sagittal, T2). Hyperintense focal contusion in the spinal cord. Rupture of the anterior and posterior longitudinal ligaments.

Fig. 2.200. b dental findings

MR images of the cervical spine (a) (sagittal. include an os odontoideum

(b) (sagillal.

T1). No bony destruction.lnci-

T2). Minimally

hyperintense

signal

alteration in the spinal cord at the level of (1 consistent with a spinal cord contusion.

67

Spinal Cord Trauma ::;< Q

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Clinical Aspects ............................................................................................ •.. Typical presentation Variable. Sudden paralysis or paresis with variable sensory deficits. In many cases late onset of clinical symptoms (days after trauma) • Bladder dysfunction. Anterior cord syndrome involves naccid paresis of the upper extremity. Posterior cord syndrome involves pain. hyperesthesia. and paresis in the arms and hands. ~ Complications Loss of central regulation. Respiratory insufficiency. Paralytic ileus. Bladder atony. Permanent neurologic damage. ~ Therapeutic options Stabilization of unstable injuries. Decompression of any focal stenosis. Highdose steroid therapy . •.. Prognosis Spinal shock is completely reversible within 72 hours. Prognosis of spinal shock and compression is highly variable and depends on many factors. Late sequelae must be expected wherever symptoms fail to improve within four weeks. Differential Diagnosis ............................................................................................ Severed spinal card

- Clinical and imaging findings

Spinal card hemorrhage

- MRIcan detect blood and its breakdown products. but only 24-36 hours after injury at the earliest! OWl may help

Selected References jarg.

J.

Menger

H. Das Halswirbelsc'iulen-

1998:21: 1307-1314

68

und Halsrnarktrauma.

Deutsches Arzteblatt

Definition ...•........................................................................................

::;I

Intramedullary accumulation of cerebrospinal nuid resulting from dilation of the central canal (hydromyelia) or paracentral cavitation (syringomyelia); these conditions are often simultaneously present and indistinguishable • Syringobulbio: Spread into the medulla oblongata. Communicating syringomyelia: Occurs in 14% of cases. Involvement of the fourth ventricle. associated with hydrocephalus. _ Congenital malformations: Chiari I malformation, encephalocele. Dandy-Walker syndrome, cysts. - Meningitis. - Intraspinal hemorrhage. Noncammunicating syringomyelia: 65% ofcases • No communication with the fourth ventricle. - Chiari I malformation. - Spinal arachnoiditis. - Tethered cord. - Cystic degenerative tumors (ependymomas. astrocytomas). - Atrophic syringomyelia (ex vacuo syringomyelia). - Lossof parenchyma from spinal trauma or infarction. _ Equally common in both sexes. Peak age; 20-40 years.

3

Q

l: Q

Imaging Signs ............................................................................................ •

Modality of choice

MRI. •

Radiographic

findings

Associated bony malformations of the spine: Atlantooccipital fusion, spina bifida, Klippel-Feil deformity. Secondary bony changes: Scoliosis, dilation of the spinal canal. degeneration, and/or destruction of the facet joints. • CTfindings

Detailed visualization of bony changes. CTmyelography: Where MRIis contraindicated. Widening of the spinal cord. Syrinx fills on late images. •

MRI findings

General: - Sagittal and axial Tl- and T2-weighted images. _ CSFnow study (at the respective level or in the other CSFspaces). _ Contrast studies are indicated in uncertain cases to exclude tumor.

_ Complete spinal cord examination: From the cervical spine including the foramen magnum (to exclude a Chiari malformation) to the lumbar spine. _ Supplementary cerebral MRIto exclude a cerebral malformation.

69

Syringohydromyelio :;i Q

<:

3

Q

2.21 o. b Spasticity, more pronounced on the left side, beginning

Fig.

several years after previous spinal trauma. MR image of cervicothoracic region

(sagittal, T2). Intramedullary cavitation from T2 to T6, widest at TS(detail, b).

T1:

Tubular to lobulated focal signal alteration in spinal cord, usually isointense to (SF, possibly partialiy septate. - Signal is occasionally hyperintense to (SF due to increased protein content. Spinal cord may be distended. T2: - Focal signal alteration in the spinal cord, usually isointense to (SF. - The pulsatile motion of the syrinx nuid produces now voids, a finding of prognostic importance as these lesions usually respond well to creation of a shunt. Clinical Aspects ............................................................................................ • Typical presentation Dissociated sensory deficits (often loss of sensitivity to pain and temperature). Radicular pain. Weakness in the extremities, sensation of stiffness in the legs. Muscle atrophy in the upper extremities.

scoliosis. 70

Neurogenic arthropathy, progressive

Brainstem symptoms where the lesion extends into the hindbrain.

Syringohydromyelia :;< Q c:

3 Q

Fig.2.22

MR image of TS (axial. T2). Ec-

Fig.2.23

MR image of the cervical spine

centric cavitation on the left side at the

(sagittal. T1) in an asymptomatic

level of 15. A fine linear structure

old man. Hypointense

extends

from the spinal cord to the dura: posttraumatic

tion.

27-yeardefect

at (7.

tethering.

Same patient as in Fig. 2.23 (sagittal. T2). Hyperintense signal alteraFig.2.24

longitudinal

Same patient as in Fig. 2.23 (sagittal. T1 with contrast). No abnormal enhancement. No Chiari I malformation. Final diagnosis: typical syrinx.

Fig.2.25

71

Syringohydromyelia :;t Q

t:

3 Q

~ Therapeutic options Treatment is indicated only for symptomatic syrinx. Decompressive laminectomy and syringotomy (posterolateral myelotomy to drain the syrinx into the subarachnoid space) • Syrinx shunting. Percutaneous needle aspiration (Caution: Syrinx may refill) • Terminal ventriculostomy: With a lumbar syrinx, the filum terminale is opened to create communication between the terminal ventricle and subarachnoid space. Patients with posttraumatic syrinx respond especially well to surgical treatment.

~ Prognosis This depends

on the underlying

cause and the severity of the neurologic

deficit.

Differential Diagnosis

............................................................................................

Cystic tumor or rumor component Selected

References

Brodbelt AR.Syringomyelia and the arachnoid web. Acta Neurochirurg (Wien) 2003: 145: 707-711 Brugieres Pet al. CSF flow measurement in syringomyelia. AJNR Am J Neuroradiol 2000: 21: 1785-1792 Di Lorenzo N et al. Adult syringomyelia: classification. pathogenesis and therapeutic approaches.J Neurosurg Sci 2005: 49: 65-72

7:1

Definition

............................................................................................ • Epidemiology Unilateral and bilateral facet joint dislocations accompany up to 50% of cervical spine injuries.

Usually they occur at (4-(6

::;l Q

c:

3 Q

• Associated fracture is present in

about 35% of all cases. • Etiology, pathophysiology, pathogenesis Traumatic rupture of the posterior cervical ligament complex (primarily the interspinous ligaments and capsule, to a lesser extent the posterior longitudinal ligament) with or without an associated bony fracture. Anterior tilting of a vertebra relative to the next caudal vertebra, opening a gap between the spinous processes. Incomplete articulation of the facet joints ("jumped facet" usually unilaterally, in severe cases bilaterally with blockage) • Subluxed vertebra may be anteriorly displaced. Flexion and rotation. Classification: Unilateral facet dislocation: Hypernexion and rotation. Rupture of the interspinous ligaments and capsule of the respective facet joint. Bilateral facet dislocation: Hypernexion with distraction. Rupture of the interspinous ligaments. Rupture of both facet joint capsules. Rupture of the posterior longitudinal

ligament

• Rupture of the annulus fibrosus.

Imaging Signs • Modality of choice Initial spiral CT is indicated with multiple trauma and extensive clinical symptoms. Otherwise conventional radiographs in two planes will suffice (not with the patient supine as this could mask signs) • MRIdemonstrates ligament structures and possible spinal cord injuries. • Radiographic findings Segmental hyperkyphosis (abrupt interruption of cervical lordosis) • Increased distance between the spinous processes ("fanning") • Focal malalignment of the facet joints in the lateral plane. Slight posterior widening or anterior narrowing of the affected disk interspace. Minimal anterior displacement may be present (1-3 mm). • CTfindings Spiral CTof the cervical spine (slice thickness 1 mm) • Sagittal reconstructions are very helpful.

Direct visualization of facet dislocation.

Anterior displace-

ment of the articular process relative to the adjacent caudal one (double facet sign) • Visualization of bony injury. • MRIfindings Tl- and T2-weighted STIR. Sagittal imaging plane. Demonstrates ligament injuries. Shows possible spinal cord injuries.

73

Anterior Subluxation

~

Q

c:

3 Q

a of the cervical spine (parasagittal reconstruction; a). The inferior articular processes of C5 lie anterior to the superior articular facets of C6. CTof C5-C6 (axial; b). Anterior subluxation with bilateral facet joint dislocation (double facet sign).

Fig. 2.260, b

Fig. 2.270, b

Conventional lateral radiograph (a). Anterior subluxation of C5-C6 with

bilateral facet joint dislocation. Spinal cord compression.

MR image of the cervical spine

(sagittal, 12; b). Anterior subluxation of C6 relative to C7 with bilateral facet joint dislocation, severed spinal cord. and flaccid paralysis.

74

Anterior Subluxation Clinical Aspects

............................................................................................ • Typic.tl presentation Severe neck pain. Restricted flexion and extension. Localized tenderness to palpation above the affected interspinous space. Neurologic symptoms are often present. •.. Complications Nerve root injury occurs in 25% of cases of unilateral facet dislocation. Spinal cord injury occurs in 25% of cases. Bilateral facet dislocation often involves severe neurologic complications (quadriplegia in 72% of cases) • Spinal cord compression with edema, necrosis, hemorrhage, and/or severance .

:;< Q

c:

3 Q

•.. What does the clinician want to know? Unilateral

or bilateral?

• Spinal cord injuries?

• Fracture?

•.. Therapeutic options Reduction may be attempted with halo traction (success 50%) • Surgical decompression is indicated for neurologic sion . •.. Prognosis Late instability with recurrent dislocation is possible after py. Slight spinal cord contusion is reversible. Other late can occur. Selected

rate approximately complications. Fu-

conservative theraneurologic sequelae

References

Galanski M. Wippermann B. Stamm G. Bazak N, Wafer A. Kompendium der traumarologischen Rontgendiagnostik. Berlin: Springer 1999 Lomoschitz F.Bildgebung bei Wirbelsaulenverletzungen - Diagnostic Imaging. Wien Med Wochenschr 2001; 151: 502-505

75

:;t Q

<:

3 Q

~~~~!~~?~

.

• Epidemiology Relatively common in people with osteoporosis. Often occult. • Etiology. pathophysiology, pathogenesis Sacral stress fracture. Relatively slight trauma or normal stresses act on deficient or abnormal bone. Predisposing factors include: - Osteoporosis. - Osteomalacia.

- Rheumatoid arthritis. - Steroid therapy. - Pelvic irradiation.

- Alcoholism. - Postoperative longstanding immobilization of the spine. Imaging

Signs ............................................................................................

• Modality of choice MRJ is suitable for diagnosing even minimal insufficiency fractures.

cr is more

suitable for directly imaging the fracture line. Bone scans can also provide valuable information although they often cannot clearly distinguish these fractures from sacroiliitis. • Radiographic findings Up to 50% of all normal traumatic sacral fractures are missed. Most insufficiency fractures cannot be detected on conventional radiographs. In rare cases, a ti-

ny fracture line will be visible. The fracture is typically located parallel to the sacroiliac joints. • Cffindings Axial thin-slice cr (maximum slice thickness 3 mm) • Coronal reconstructions. Direct visualization of the fracture line. Local destruction of cancellous bone without a fracture line is a sign of microtrauma

• Osteopenic bone structure.

• MRI findings STIR(coronal) • Tl (axial. coronal) • Bone marrow edema is visualized on the STIRsequence. The fracture line is occasionally visualized on Tl-weighted images. Other causes for clinical symptoms are visualized. Clinical Aspects

............................................................................................

• Typical presentation Low back pain. Radiates into buttocks or thigh. Neurologic deficits are rare. History includes only slight trauma or none at all. • What does the clinician want to know? Exclude other possible causes of clinical symptoms.

76

Insufficiency Fracture

of the

Socrum ::;t Q c:

3 Q

Fig. 2.280, b

P-A bone scan of the pelvis and sacrum (a). Increased tracer uptake

around both sacroiliac joints in typical butterfly pattern. MR image of the sacrum (axial, T1: b). linear insufficiency fracture of the left sacrum.

Fig. 2.290. b

CT of the sacrum (coronal) (a). Bilateral insufficiency fractures of the sacrum. Cortical discontinuity with minimal local fracture of the cancellous bone. MR image of the sacrum (coronal, proton density fat-saturated; b). Diffuse bilateral bone marrow edema in the sacrum, an indirect sign of insufficiency fracture.

77

Insufficiency Fracture of the Socrum :;t Q

<:

3 Q

~ Therapeutic options Treatment is invariably conservative. Bed rest and pain management are important in the initial phase. Later. the patient should be mobilized as quickly as possible (especially in osteoporosis] • Preventative osteoporosis therapy. low dose of corticosteroids • Physical therapy. ~ Prognosis Patients are usually free of pain within four weeks. Differential Diagnosis Metastases Sacroiliitis Lumbar radiculopathy

-

MRIor cr can directly visualize metastases History of malignancy Erosive changes in the sacroiliac joints Disk protrusion or extrusion Spondylolisthesis

Selected References Konig A. Insuffizienzfraktur des Os ileum und des Os sacrum. Z Rheumatol 2000: 59: 343-347 Weber M, Hasler P, Gerber H. Insufficiency fractures of the sacrum. Spine 1993; 18: 2507-2512

78

~!!?i.t!?~.~~~~~~/~/!.~~~,. ~~~~~~!~!~~~~.~~~~! . ::;tc: Q

~ Epidemiology Affects about 4.5% of children at 6 years of age. Affects about 6% in adulthood. Men are affected more often than women. In competitive athletes playing sport involving repetitive lordosis. the rate increases to about 50% • Predisposing disorders include Marfan syndrome. osteogenesis imperfecta. and osteopetrosis. ~ Etiology, pathophysiology, pathogenesis Stress reaction. Stress fracture - spondylolysis. Competitive sport at an early

3 Q

age involving repetitive reactions to stresses from muscle contraction, weight

bearing, and rotational forces leads to a defect in the pars interarticularis • Spondylolysis can lead to slippage of the adjacent cranial vertebra (spondylolisthesis). Unilateral (about 15%of cases) or bilateral spondylolysis. Meyerding clossificotion of spondylolisthesis: - Grade I: Anterior slippage of the adjacent cranial vertebra by less than 25%. - Grade II: Anterior slippage by 25-50%. - Grade III: Anterior slippage by 50-75%. - Grade IV:Anterior slippage by 75-100%. Imaging

Signs ............................................................................................

~ Modality of choice Only MRIcan demonstrate the stress reaction (cancellous fracture) • However. a stress fracture can be difficult to detect on MR images. Therefore, the modality of choice for imaging stress fractures is conventional radiography (oblique view) or, in uncertain cases, spiral

cr •

MRI alone is indicated in children and adoles-

cents (to limit exposure to ionizing radiation). ~ Radiographic findings Spondylolysis is more readily detectable on oblique films than on lateral films. Visible as a defect in the "neck" of the "Scottie dog." ~ CTfindings

cr

with a maximum slice thickness of 2 mm • Sagittal reconstructions.

Direct

visualization of a fracture line. Caution: Findings can mimic an additional facet joint. ~ MRI findings Sagittal T1-weighted and STIRsequences. Additional axial sequences are indicated in the affected segments. Edema sign. Cancellous fracture line (no correlate on CT or conventional radiographs) • Axial slices show widening of the spinal canal.

Reduction in the perineural fatty tissue at the nerve roots.

Focal

hypointensity in the pars interarticularis on axial Tl- and T2-weighted sequences.

79

Stress Phenomena in the Spine :;i Cl

<:

3 Cl

Fig.2.30

MR image of L3 (axial. T2).

Bone marrow edema in the right vertebral

arch (chronic stress) with effusion in the facet joint (baseball player).

Fig.2.32 a of vertebra l3 (axial). Spondylolysis with visible asymmetrical defects in both laminae.

80

Fig. 2.31 MR image of l3 (axial. T2). Bone marrow edema in the right vertebral arch from chronic stress (baseball player).

Fig.2.33 Conventional lateral radiograph of the lower lumbar spine. Defect in the vertebral arch with anterior slippage of the vertebra (spondylolisthesis). Meyerding stage IV (- SO%).

Stress Phenomena in the Spine Fig.2.34

Fig.2.35

Conventional

lateral radio-

graph of the lumbar

spine (detail).

Pseu-

dospondylolisthesis

in disk degeneration.

:;i

o c:

3 o

Meyerding classification of spondylolisthesis.

81

Stress Phenomena in the Spine Clinical Aspects ............................................................................................ ~ Typical presentation Often asymptomatic in children. Later chronic low back pain is often present • Pain increases with exercise. Radiculopathy is present in higher grade spondylolisthesis. ~ Complications Neurologic symptoms. ~ Therapeutic options Treatment in most cases is conservative. Surgical treatment (posterolateral fusion) is indicated only in patients with spondylolisthesis of any grade where neurologic symptoms are present. ~ Prognosis Conservative therapy has a success rate of up to 70% • Neurologic deficits persist in up to 10%of cases following spinal fusion. Differential Diagnosis Partial facetectamy Pseudaspandylalisthesis

- History - Associated with marked degenerative changes in the lumbar spine - History of underlying malignant disorder

Osteogenic metastases (MRI)

Healed spandylolysis

- Signal loss in the pars interarticularis due to sclerosis -Cf

(MRI)

Selected References Brossmann

J. Czerny

Ch. Freyschmidt

J. Crenzen

gischen in der Radiologie des kindlichen

des Normalen

und erwachsenen

und Anfange des PatholoSkeletts. Stuttgart: Thieme

2001 Cassas KJ.Cassettari-Wayhs

A. Childhood and adolescent

sports-related

overuse injuries.

Am FamPhysician2006: 73: 1014-1022 Stabler A, Paulus R, Steinborn

M. Bosch R. Mathko

N. Reiser M. Die Spondylolyse

im Stadi-

um der Entstehung: Diagnastischer Beitragder MRT.R5Fo2000: 172:33-37 WilsonJB

et a!. Spinal injuries

in contact

sports. Curr Sports Med Rep 2006:

5: 50-55

Wittenberg RH.Willbruger RE.Kramer j. Spondylolyse und Spondylolisthese. Diagnose und Therapie. Orthopade 1998: 27: 51-63

82

:;i

Definition

Q

c:

The diskovertebral region is often affected (Andersson lesion of the noninflammatory type). Pseudarthrosis results where the fracture continues into the posterior elements and the ossified ligaments are discontinuous.

3 Q

Imoging Signs • Modality of choice Because of the low sensitivity of conventional radiography. multislice IT is indicated • MRI is indicated in the presence of neurologic symptoms to exclude spondylodiskitis. • Radiographic findings Low sensitivity. Discontinuity of the ossified ligaments. • ITfindings Excellent visualization of bony structures. Visualization of the typical sclerosis at the pseudarthrosis. • MRI findings In addition to purely bony changes. MRIalso demonstrates the fibrous and fibrovascular tissue typical of pseudarthrosis. which is located primarily in the diskovertebral area and facet joints.

Enhancement

after contrast administration.

Clinical Aspects

............................................................................................ • Typical presentation Ankylosing spondylitis. • Therapeutic options No consensus. ments.

Back pain.

Conservative

Instability.

or surgical.

Spinal fusion involving several seg-

Differential Diognosis Spondy/odiskitis

- Involvement

of the posterior vertebral elements

and integrity of the anterior longitudinal ligament suggest pseudarthrosis Selected References Rasker Jj. Prevo RL. Lanting PJ.Spondylodiscitis in ankylosing spondylitis. innammation trauma? A description of six cases. Scand J Rheumarol 1996; 25: 52-57 Shih IT. Chen PQ. Li YW. Hsu CY. Spinal fractures and pseudoarthrosis

complicating

or an-

kylosing spondylitis: MRI manifestation and clinical significance. JCAT2001: 25: 164-170 Trent G. Armstrong GW, O'Neil J. Thoracolumbar fractures in ankylosing spondylitis. High-risk injuries. ClinOrthop 1988; 227: 61-66

83

Stress Fractures in Ankylosing Spondylitis

:;t Q

c:

3 Q

Flg.2.36 CT reconstruction (sagittal). Pseudarthrosis from a stress fracture through all three columns in ankylosing spondylitis.

Flg.2.37 CT reconstruction (coronal). The vertebral and disk components of the pseudarthrosis are visualjzed.

84

Stress Fractures in Ankylosing Spondylitis Flg.2.38 CT reconstruction (coronal). Pseudarthrosis in the posterior spine is visualized.

:;< Q c:

3 Q

Fig.2.39 MR image of the thoracic spine (sagittal. T2). Pseudarthrosis from a stress fracture in ankylosing spondylitis. Sclerosis in the fracture lones.

85

Stress Fractures in Ankylosing Spondylitis ::;t Q c:

3 Q

86

Fig.2.40 MR image of the thoracic spine (Tl with contrast and spectral fat saturation). Axial view of the thoracic spine. Contrast uptake by the soft tissues.

Definition

............................................................................................ ~ Etiology, pathophysiology, pathogenesis Wear resulting from aging and/or overuse, and other unknown causes. Associated with Scheuermann disease. There is dehydration with subsequent loss of function of the disk structures (primarily partial radial tears in the fibers of the annulus fibrosus. leading to broad-based disk bulge or protrusion) • Loss of height and deformation of the disk. Displacement of parts of the nucleus pulposus within the disk (T2 hyperintensity). Chronic overuse and abnormal stress results in wear and disturbs the supply of nutrients to the disk (loss of water and proteoglycans). This in turn leads to loss of tissue function and integrity (concentric and/or transverse fiber tears in the annulus fibrosis) and ultimately to disk deformation. Schmorl node: Circumscribed defect in the superior or inferior end plate leading to disk herniation. Etiology: Presumably osteonecrosis with insufficiency fracture.

Nucleus pulposus: Gelatinous material with high water content in the center of the intervertebral disk. Annulus fibrosus: Consists mainly of fibrocartilaginous material and concentrically arranged collagen fibers. Imaging Signs

............................................................................................ ~ Modality of choice MRI(sagittal, T1 and T2) • Height reduction.

Signal loss on water-sensitive se-

quences.

~ Radiographic findings Height reduction in the disk interspace. body (close to the disk) with sclerosis. ~ CTfindings Height reduction. becular structure.

Deformation.

Scll/norl nodes: Defect in the vertebral

Schmorl nodes: Sclerotic margin. normal tra-

~ MRI findings Dehydration (T2 hypointensity) • Height reduction. Displacement of portions of the nucleus pulposus (T2 hyperintensity) into the annulus fibrosus (T2 hypointensity) • Deformation (broad. intraligamentous disk bulge: annulus fibrosus is intact) • Schmorl nodes: - Acute: Edematous halo. - Chronic: Sclerotic halo with conversion of fatty marrow. Clinical Aspects ~ Typical presentation Usually asymptomatic (75% of cases) • Nonspecific low back pain. Lossoffunction with limited motion in the spine.

Degenerative disk disease.

87

Disk Degeneration ~

':il ~

fig. 3.1 Conventional radiograph (specimen). Schmorl node in the inferior endplate with fine marginal sclerosis chronic Schmorl node) .

a..• (-

,,' III

o

;;;.

o

a. III

;;:

fig.3.2 MR image of thoracolumbar junction (STIRsagittal). Reduced disk height is indicative of degeneration. Circumscribed impression of the superior and inferior end plates of L1 and L2 with disk protrusion (Schmorl node).

88

Disk Degeneration

Fig. 3.30, b MR image of the lower thoracic and lumbar spine (sagillal, T2. Tl). Tl and T2 showing a disk impression in the posterior half of the superior endplate and surrounding fatty marrow (- subacute Schmorl node) .

• Therapeutic options Acute low bock pain: Analgesia. Physical therapy. specific back exercises. rection of posture. Strengthening of the local musculature.

Cor-

Different;oID;ognos;s

............................................................................................ Nondiskogenic bock pain

Protrusion, extrusion. sequestration Diskitis. spondy/odiskitis Schmorl node Chorda remnant

- Osteoporotic or pathologic vertebral coliapse - Lying in dorsal part. No other degenerative changes!

Selected References Bohndorf K. Imhof H. Radioiogische Diagnostik der Knochen und Gelenke. 2nd ed. Stutt-

gart: Thieme 2006 Modic MT. Degenerative disc disease and back pain. Magn Reson Imaging C1in N Am 1999; 7:481-491 Morgan S. MRI of the lumbar intervertebral disc. Clin Radial. 1999: 54: 703-723 Schmorl

G. Ober Knorpelknotchen

an den Wirbelbandscheiben.

1929: 38:265 Vahlensieck M, Reiser M. MRT des Bewegungsapparates,

Fortschr R6ntgenstr

3rd ed. Stuttgart: Thieme 2006

89

Definition

............................................................................................

~ Etiology, pathophysiology, pathogenesis Initial stage of degenerative disk disease. Edema of the adjacent subcortical portions of the vertebral body in disk degeneration with decrease in fluid content and loss of disk height, usually in the lower cervical and lumbar spine. Pseudoinflammatory • Most likely a reactive change to abnormal stresses. Microangiopathy • Hyperemia. Endothelial damage. Fluid leakage. pseudoinflammatory or inflammatory reaction, ingrowth offibrovascular tissue. General picture of edema. Imaging Signs

............................................................................................

~ Modality of choice - Conventional A-P and lateral radiographs. - MRI(sagittal. STIR,n. and axial to exclude disk herniation). ~ Radiographic findings Loss of disk height. Postural deficiency. ~ MRI findings Cancellous bone adjacent to the inferior and superior endplates of the affected segment appears hyperintense on Tl-weighted images and hypointense on T2weighted images. consistent with vasogenic bone marrow edema. Disk is darker on T2-weighted and STIRimages. consistent with fluid loss. Clinical Aspects

............................................................................................

~ Typical presentation Lumbago. Cervical spine pain. Painful edema. Often multiple spinal regions may be symptomatic. including symptoms of facet joint degeneration. ~ What does the clinician want to know7 Exclude spinal stenosis or stenosis of the neural foramina. Exclude spondylodiskitis • Exclude malignancy. ~ Therapeutic options Conservative with physical therapy. Analgesia where indicated. ~ Prognosis Progression to Modic II (often within 7-9 months).

90

Degenerative Disk Disease-Modic

I

flg.3.4 MR image of the lumbar spine (sagittal. STIR).L5-S1 shows hyperintensity adjacent to the disk (edema). The disk is hypointense with reduced height. Posterior herniation with intact posterior longitudinal ligament.

flg.3.5

Modic type I degenerative disk

disease. MR image of the lumbar spine

(sagittal. 12). Disk height is reduced. Posterior disk herniation. Subcortical hypointensity with fine hyperintense halo (edema and beginning fatty marrow conversion).

91

Degenerative Disk Disease-Modic

I

Differential Diagnosis Diagnosis is obvious in

most cases Spondylitis, spondylodiskitis

- History - Disk shows hyperintensity and may show increased volume - Irregularly demarcated from disk - (ontrast adminiseration

Atypical hemangioma

-

Status post recent vertebral fracture

- History - May be difficult to differentiate after recent fracture - Height reduction in the vertebral body limited to the affected vertebra - Fluid signal in vertebra - Diffusion-weighted sequence

Selected

Rarely confused More central location Tends to be round and limited to the affected vertebra Also resembles edema Increase in longitudinal trabeculae on plain radiographs and CT

References

Modic MT. Degenerative disc disease and back pain. MRI Clin N Am 1999; 7: 481 Modic MT. Steinberg PM. Ross JS. Masaryk TJ. (arter JR. Degenerative disc disease: assessment of changes in vertebral

bone marrow

with MR Imaging. Radiology

193 Vahlensieck M. Reiser M. MRT des Bewegungsapparates,

92

1988; 166:

3rd ed. Stuttgart: Thieme 2006

Definition

",o ",:J ",..., o ~ ~. ", o ;;;.

lC

~ Etiology, pathophysiology, pathogenesis Degenerative disk disease with fatty degeneration of the cancellous bone adjacent to the end plates (stress-induced conversion of fatty marrow) • There is progressive fatty degeneration of the pseudoinflammatory area of the vertebra (Modic I) • Often occurs in the lower lumbar and lower cervical spine. See Modic I. Imaging Signs

o ...,

0..

",;;:

............................................................................................ ~ Modality of choice Conventional radiographs. MRI: sagittal (STIR.T1) and axial (TI). ~ Radiographic findings Reduced disk height. Postural deformity. Osteophytes may limit mobility on stress radiographs. ~ MRI findings There is a hyperintense area in the vertebral body adjacent to the disk on Tlweighted and T2-weighted images. appearing hypointense on the fat-suppressed sequence. Height reduction and increasing fluid loss in the disk. which appears hypointense on the T2-weighted and STIRsequences. Often associated with osteophytes, which occasionally mask bulging of the degenerative disk. Clinical Aspects

............................................................................................ ~ Typical presentation Pain decreases as the Modic I edema recedes. This finding is pathognomonic. ~ Therapeutic options Physical therapy to strengthen the back musculature and stabilize the spine. Surgical aptians: Spinal fusion or prosthetic disk. Differential Diagnosis

Posttraumatic vertebral fracture

- An older fracture may show fatty degeneration but not sclerosis

Hemangioma

-

Limited to the affected vertebra History Typical hemangioma also shows fat-equivalent signal Tends to be round and limited to the affected vertebra Visible trabeculae on cr. occasionally on MRIas well

Liposarcoma

- Very rare

93

Degenerative Disk Disease-Modic

:i? ~

i6

a...•

Flg.3.6 MR image of the lumbosacral region (sagittal. T2). Markedly hyperintense subcortical band due to fatty marrow conversion .

<' III

o

(;;'

o

f} i:l

Fig. 3. 7

MR image of the lumbosacral region (sagittal, STIR).Subcortical hyperintensity adjacent to the disk due to fatty marrow conversion. The disk is also hyperintense. The superior and inferior endplates are irregular, with tiny Schmorl nodes.

94

/I

Degenerative

Selected

Disk Disease-Modic

/I

References

Modic MT. Degenerative disc disease and back pain. MRI C1in N Am 1999; 7: 481 Modic MT, Steinberg PM, RossJS.Masaryk TJ.Carter JR. Degenerative disc disease: assessment of changes in vertebral

bone marrow with MR Imaging. Radiology 1988; 166:

193 Vahlensieck

M. Reiser M. MRT des Bewegungsapparates.

3rd ed. Stuttgart:

Thieme 2006

95

Definition • Epidemiology Reactive stiffening in the setting of spinal degeneration and abnormal mobility with increasing age (40-60 years) • More common in men than woman. More common with short pedicles • More pronounced on the concave side of scoliosis or asymmetry. more often on the right than left (probably due to the aorta) • Predilection for the lower lumbar spine. middle and lower cervical spine. and thoracolumbar junction. • Etiology, pathophysiology, pathogenesis Multisegmental osteophytes (horizontal. handlelike. etc.) • Modic 11/:Transformation of the Modic II fatty degeneration into subcortical sclerosis. Reactive osteophytic proliferation in the setting of spinal degeneration (tension and compression. metabolic), creating functionally fused vertebrae • Outgrowths begin beneath the margin on the endplates, especially at the insertion of the anterior longitudinal ligament • Maximal severity: Bridging osteophytes. Significance:

- Especially if posterior: Narrowing of the spinal canal. - Lateral and posterolateral orientation: Narrowing of the neural foramina. - With severe anterior osteophytes: Role in the development of aneurysms.

Imaging Signs • Modality of choice - Conventional A-P and lateral radiographs. stress radiographs where indicated. - Where imaging findings are equivocal and conflict with clinical findings: supplementary MRI. • Radiographic findings Increased subchondral sclerosis. Osteophytes adjacent to the end plates • Bizarre configurations of proliferative and bridging osteophytes. • CTfindings As on radiographs. Narrowing of the spinal canal and bony neural foramina is better visualized. • MRI findings Low subchondral bandlike intensity (- subchondral sclerosis). Sagittal images often show multisegmental spinal osteophytes with obliteration of the subarachnoid space and perineural fatty tissue. The high soft tissue contrast is best for evaluating the overall situation. as the improved visualization of neural structures helps to identify secondary radiculopathy and myelopathy. Usually there are other signs of spinal degeneration. Significance of narrowing of the bony neural foramina and spinal canal is usually overestimated. For selected normal values of spinal canal width. see Disk Protrusion, p. 100.

96

Fig.3.8a,b Conventional radiographs of the lumbosacral junction (A-P. and lateral b). Numerous lateral and anterior osteophytes, some growing in hairpin or beaklike shapes.

Fig.3.9 Conventional lateral radiograph of the cervical spine. Marked bridging spondylosis deformans and degenerative disk disease, with reduced disk height and osteophytes. Modic III,with reduced disk height and subcortical sclerosis.

97

Spondylosis

t:l

Deformons-Modic

III

Modic I

~

Modic II

Modic III

'"

::l

'"a..• ~.

T1

t:l

;;;. 0

a..

'" <:l

T2

Fig.3.10 Subchondral degenerative conversion. Modic III - sclerosis.

Fig.3.11

Conventional lateral radio-

graph of L3-L4. Spondylosis

degenerative disk disease.

98

changes:

with severe

Modic I = edema.

Modic 11- fatty marrow

Spondylosis Deformons-Modic

/1/

Clinical Aspects

............................................................................................ • Typical presentation Ranges from asymptomatic to severe pain: rarely correlates with radiographic findings. Other disorders are often excluded based on radiographic findings. In particular. these include stenosis of the spinal canal and neural foramina. other degenerative spinal disorders such as spondylarthritis. synovial cysts. uncovertebral osteoarthritis of the cervical spine. disk displacement. abnormal mobility with pseudospondylolisthesis, and thickening of the ligamenta f1ava • Narrowing of the neural foramina will also involve segmental symptoms . • Therapeutic options Lumbago is managed with analgesics and infiltration of pain relieving drugs. Physical therapy to strengthen the back musculature. ete. • Neurologic symptoms such as paraplegia and bladder paralysis require surgical decompression (foraminotomy. laminectomy. hemilaminectomy. fusion).

o

'" :'"l '...•o..•"

10

,,' ';;;." o o ...•

0..

;';1"

Differential

Diagnosis ............................................................................................

Syndesmophytes

- History - With progressive inflammatory disorders (especially ankylosing spondylitis) - Growth is vertical and initially thin

Pamsyndesmophytes

- Occur in inflammatory and Reiter syndrome - Typically asymmetric.

disorders

such as psoriasis

thicker than syndesmophytes.

extend in an arc outward from vertebra Vertebml collapse with displacement of anterior or posterior margin

- Osteopenic bone structure - Wedge or fishlike vertebrae

Ligament calcifications

- OPLL(ossified posterior - DISH (diffuse idiopathic - Rare

Selected

longitudinal ligament) skeletal hyperostosis)

References

Bohndorf K. Imhof H. Radiologische Diagnosrik der Knochen und Gelenke. 2nd ed. Stuttgart: Thieme 2006 Dihlmann W. Joints and vertebral connections. Stuttgart: Thieme 1985 MolierT. Reif E. CT- und MRT-Normalbefunde. Stuttgart: Thieme 1998 Resnick. D. Niwayama G (eds.). Diagnosis of Bone and Joint disorders. 3rd ed. Philadelphia: Saunders 1995 Vahlensieck M, Reiser M. MRT des Bewegungsapparates, 3rd ed. Stuttgart: Thieme 2006

99

Definition (American Society of Neuroradiology) ............................................................................................ Bulge: > 50% of the disk circumference (not a hernia). Herniation: Bulging of disk material past the margins of the intervertebral space « 50% of the disk circumference). - Protrusion: Broad communication between hernia and disk ("broad-based" -25-50%, "focal" = < 25%). - Extrusion: Necklike (hourglass-shaped) communication between hernia and disk. - Sequestration: Herniated disk material separated from the central disk. It can migrate cranially or caudally. Caution: The term "prolapse" should no longer be used as it is not consistently defined. Localization of the herniation: Central.

Central ipsilateral.

Subarticular • Foraminal • Extraforaminal (axial

image). At disk level. Infrapedicular • Pedicular. Suprapedicular (lateral image). Nucleus pulposus: Gelatinous material with high water content in the center of the intervertebral disk. Annulusfibrosus: Composed mainly of fibrocartilaginous material and consists of concentrically arranged collagen fibers. Chronic overuse and abnormal stress results in wear and disturbs the supply of nutrients to the disk (loss of water and proteoglycans). This in turn leads to loss of tissue function and integrity (concentric and/or transverse fiber tears in the annulus fibrosis) and ultimately to disk deformation. Increased risk of hernia or bulge. Imaging Signs ............................................................................................ • •

Modality of choice MRI. Radiographic findings

Height reduction in the disk interspaces. • CTfindings

Circumscribed bulging of disk material (isodense to soft tissue) • Disk material in the lateral recess (displacing the fatty tissue) • Sagittal reconstruction (multidetector CT) • Vacuum phenomenon. •

MRJ findings

Circumscribed disk deformation extending beyond the posterior longitudinal ligament. Displacement of parts of the nucleus pulposus within the disk (T2 hyperintensity) • Disk contour (axial and sagittal) • Relationship to dural sac (displacement. deformation, myelopathy). spinal stenosis • Relationship to the nerve roots (perineural fatty tissue. contact, displacement) • Neuropathy _ nerve foot thickening and signal alteration.

Neural foramen stenosis. Vacuum

phenomenon (Tl hypointensity, T2 hypointensity).

100

Disk Herniation

OD Protrusion

Extrusion

.?~.r!!.~ p.~~ ~~_~_I~ ~. Pedicular

Infra pedicular ••••••••

_nonn

••••••••••

Oiskal

Fig.3.12a-d Disk herniation. Asymmetric "bulging" (a). protrusion and extrusion (b), anatomic position of disk hernias in the axial imaging plane (e) and sagittal plane (d).

Fig.3.13 MR image of T12 (axial. T2). Marked dehydration of the disks in the thoracolumbar junction with broadbased intraligamentous disk protrusions in the left lateral region « 50% of the circumference).

101

Disk Herniation Clinical Aspects • Typical presentation Usually asymptomatic • Nonspecific, nondiskogenic back pain. Typically, pain at the level of the disk, intensity of pain increased with coughing and pressing. Characteristic sensory and motor deficits . • Therapeutic options Acute low back pain: Analgesia. Physical therapy, specific back exercises. Correction of posture • Strengthening of the local musculature. Surgery is indicated only if several attempts at conservative therapy are unsuccessful (except in the presence of distal neurologic deficits, or bladder or rectal paralysis).

Differential Diagnosis ............................................................................................ Disk bulge Nandiskogenic

- > 50% of the circumference of the vertebra: disk bulge and not herniation spinal

stenosis or neural foraminal stenosis Diskitis

- Osteophytes - Facet joint degeneration with marked proliferation of osteophytes and hypertrophy of the ligamenta nava -

Entire disk hyperintense on T2-weighted images Associated bone marrow edema Soft tissue component Increased innammatory markers (does not invariably occur)

Selected References Bohndorf K. Imhof H. Radiologische Diagnostik der Knochen und Gelenke. 2nd ed. Stuttgart: Thieme 2006 Greenspan A. Orthopedic Radiology. A Practical Approach. 3rd ed. Philadelphia: Lippincott Williams and Wilkins 2000 Luoma K: low back pain in relation to lumbar disc degeneration. Spine 2000; 25: 487-492 Milerre

PC. Differentiating

lumbar

disc protrusions,

disc bulges. and discs with

normal

contour but abnormal signal intensity. Magnetic resonance imaging with discographic correlations.

Spine 1999: 24: 44-53

Moulopoulos lA. MR prediction of benign and malignant vertebral compression fractures. J Magn Reson Imaging 1996; 6: 667-674 Pardon OF. Milette PC. Nomenclature and Classification of lumbar Disc Pathology. Spine 2001: 26: E93-113 Vahlensieck M. Reiser M. MRT des Bewegungsapparates, 3rd ed. Stuttgart: Thieme 2006

102

Definition ............................................................................................ • Epidemiology L5-S1 is most often affected. Note: Up to 50%of patients over 50 years may have asymptomatic disk protrusions and extrusions that often resolve within 9-12 months ("physiologic aging" of the disk). • Etiology, pathophysiology, pathogenesis Rupture ofthe annulus fibrosus with circumscribed transligamentous bulging of the disk material (mainly portions of the nucleus pulposus, hyperintense on Tlweighted images). Extrusion: Disk material is primarily displaced posteriorly. The largest diameter of the displaced disk material is larger than its diameter where it exits the interspace, creating a "neck" of displaced material. Sequestration: Lossof continuity of the disk with displacement of portions of the nucleus pulposus, which migrate either through the ligament to lodge against the dura or within the ligament along the posterior margin of the vertebra. The migrating tissue has no connection with "mother" disk. Separation of disk material.

Imaging Signs ............................................................................................ • Modality of choice - MRI(sagittal. axial). - Cf (where MRIis not available or contraindicated), • Radiographic findings Nonspecific (reduced height of disk interspaces) • Disk calcification (65% of cases) • Vacuum phenomenon.

• Cffindings Bulging of disk material (isodense to soft tissue) • Disk material in the lateral recess (displacing the fatty tissue) or along the posterior margin of the vertebra, suggesting sequestration (sagittal reconstruction with multidetector Cf) • Calci•

fication • Vacuum phenomenon. MRI findings

Position relative to posterior longitudinal ligament • Discontinuity of disk. Subligamentous or transligamentous bulging of disk material (isointense to soft tissue) • Position relative to dural sac (displacement, deformation, myelopathy), spinal stenosis. Position relative to nerve roots (contact with or displacement of perineural fatty tissue: neuropathy appears as thickening and signal alteration of

the nerve root) • Neural foraminal stenosis. spine (sequestrum)

Separated disk material within the

• Marginal contrast enhancement.

Accompanying vacuum

phenomenon is proof of degeneration. Caution: Where spinal stenosis is presenr. (SF signal loss often occurs in the adjacent anatomy. This signal void due to flow turbulence can mimic a seques-

trum • MRIfindings should be correlated with the clinical findings,

103

Bulge, Protrusion, Extrusion, Sequestration Fig.3.14 Schematic diagram (axial). Broad-based protrusion of disk material. The outer part of the annulus fibrosus is torn, allowing the nudeus pulposus to protrude. Entrapment of the dural sac with displacement of the fibers of the cauda equina (protrusion).

MR image of the lumbosacral region (sagittal, T2). Posterior transligamentous disk herniation with a neck of displaced disk tissue (extrusion at the level of the disk).

Fig.3.15

104

Bulge, Protrusion, Extrusion, Sequestrotion Fig. 3.16

MR image of the lumbar

spine

(sagittal,

12). Cranially displaced disk

material

(sequestration).

Fig.3.17

MR image of the lumbar

(axial, 11). Circumscribed

broad·based

spine

right ipsilateral

trans ligamentous

disk

herniation at l5 with displaced nucleus

pulposus tissue in contact with the dural sac (disk protrusion).

105

Bulge. Protrusion. Extrusion. Sequestration

o ~

'" "" 'a..•

MRimage of L3(axial,T2). Posterior sequestrum from l3.

Flg.3.18

.,. '" o i:;' Q

~ <::l

Clinical Aspects ~ Typical presentation Low back pain. Radicular pain. Caution: In the presence of motor deficits. bladder paralysis, and rectal paralysis a neurosurgeon or neurologist should be consulted about whether surgery is indicated. ~ Therapeutic options This depends on the site of the extruded disk material (median, mediolateral, foraminal, or extraforaminallocation) • In most cases (90%). symptoms disappear within 4-8 weeks. Like protrusion, disk extrusion in patients over 50 is mostly asymptomatic (renecting physiologic aging of the disk) • Imaging findings should be correlated with clinical findings. Sequestration: Depends on clinical findings: sequestration can resolve spontaneously • Acute low bock pain: Analgesia. NSAlDs.corticosteroids • 8ed rest (controversial) • Physical therapy, specific back exercises. Correction of posture. Strengthening of the local musculature. Pain resistant to conservative therapy and/or neurologic deficits are treated by diskectomy. chemonucleolysis, or laminectomy.

106

Bulge, Protrusion, Extrusion, Sequestrotion Differential Diagnosis

............................................................................................ Nondiskogenic spinal stenosis or neural faraminal stenosis

- Osteophytes - Facet joint degeneration with marked proliferation of osteophytes and hypertrophy of the ligamenta flava

Epidural fibrasis

- Postoperative

- Homogeneous enhancement Schwannoma

Selected References Bohndorf K. Imhof H. Radiologische Diagnostik der Knochen und Gelenke. 2nd ed. Stuttgart: Thieme 2006 Greenspan A. Orthopedic Radiology. A Practical Approach. 3rd ed. Philadelphia: Lippincott Williams and Wilkins 2000 Moller. Reil. 0- und MRT-Normalbefunde. Stuttgart: Thieme 1998 Pardon DF. Milette Pc. Nomenclature and classification of lumbar disc pathology. Spine 2001; 26: E93-113 Vahlensieck M. Reiser M. MRT des Bewegungsapparates. 3rd ed. Stuttgart: Thieme 2006 Yasuma T. The histology oflumbar intervertebral disc herniation. The significance of small blood vesseis in the extruded tissue. Spine 1993; 18: 1761-1765 Zollner J. Radiological assessment Orl055 of disk height in acute and chronic degenerative lumbar disk changes. Rofo 2001; 173: 187-190

107

Definition • Epidemiology Disk displacement occurs in 5-6% of people aged over 50 years. Disk calcifications are more common in the thoracic spine. In children. they are not uncommon in the cervical spine (most likely a posttraumatic condition). • Etiology, pathophysiology, pathogenesis Disk degeneration results in release of gas (nitrogen) from the disk material (vacuum phenomenon) • The vacuum phenomenon is pathognomonic of disk degeneration and occurs in the lower lumbar and cervical spine.

Disk degenera-

tion can also result in calcium deposits (hydroxylapatite. calcium pyrophosphate), usually in the annulus fibrosus, rarely in the nucleus pulposus. Imaging Signs

............................................................................................

• Modality of choice Conventional radiographs or CT • Radiographic findings A-Pand lateral. The vacuum phenomenon shows gas density and is mostly limited to the disk. Disk calcification appears as either spurlike or homogeneously dense calcification in the disk (usually the annulus fibrosus). • CTfindings The signs are the same as on conventional radiographs. • MRI findings The gas is hypointense on T1 and T2 • The calcifications are typically hypointense on Tl and T2. Clinical Aspects

............................................................................................

• Typical presentation See p. 87 • Usually asymptomatic. • Therapeutic options See p. 89. Differential Diagnosis Disk calcification

- Metabolic disorders (chronic pyrophosphate disease. hydroxylapatite. gout. diabetes. hyperparathyroidism, etc.) - Posttraumatic

Vacuum phenomenon

- Caution: bowel may be superimposed

Selected References Bullough PC,Boachie-AdjeiO.Atlas of Spinal Diseases.Philadelphia: JBLippincott 1998

108

Disk Calcification and Vacuum Phenomenon

fig.3.19a,b Conventional lateral radiographs of the lumbar spine. Reduced disk height at L2-$' with vacuum phenomenon in each disk. Other findings include subchondral sclerosis (Modic III) and pseudospondylolisthesis at L4-L5 (Meyerding grade I) with osteophytes. Posterior osteophytes at L2-L3.

109

Disk Calcification and Vacuum Phenomenon

o ~ ~

a'" ~.

Conventional lateral radiograph of the lumbar spine (specimen). Disk narrowing at L3-l4. Marked disk calcification is seen at L2-l3 and l4-LS. Pseudospondylolisthesis at L3-l4.

Flg.3.2a

'o " i;;. o

* ::!

Fig. 3.21

Conventional lateral radiograph of Ll-l2 (detail). Disk calcification. Schmorl nodes in the superior end plate of l2.

110

of the Facet Joints) ............................................................................................

Definition (Spondylarthritis, Osteoarthritis

• Epidemiology Occurs in the setting of degenerative spinal disease with increasing age (almost invariably present in people over 60 years of age). • Etiology, pathophysiology, pathogenesis Facet joint degeneration, osteoarthritis of the facet joints. In the selling of degenerative spinal disease. reduced disk height and a consequent shift in the axis with disk degeneration lead to pseudospondylolisthesis and abnormal stresses that in turn cause facet joint degeneration. Scoliosis and asymmetry also influence facet joint degeneration, and vice versa.

Imaging Signs ............................................................................................ • Modality of choice Conventional A-P, lateral. and oblique radiographs. radicular symptoms are present. • Radiographic findings Typical signs of osteoarthritis

MRIor IT indicated when

of a synovial joint with joint space narrowing. mar-

ginal osteophytes, subchondral sclerosis and cysts, deformation. and synovial cysts. The stress view shows functionally fused vertebrae and increased mobility in adjacent segments. • CTfindings Typical signs of osteoarthritis

of a synovial joint with joint space narrowing, oc-

casional vacuum phenomenon, marginal osteophytes. subchondral sclerosis. subchondral cysts. and deformation. • MRI findings Typical signs of osteoarthritis

of a synovial joint with joint space narrowing, car-

tilage damage. marginal osteophytes, subchondral sclerosis, and occasionally effusion (or a synovial cyst), subchondral cysts, and deformation. Lateral recess >4-Smm.

Clinical Aspects • Typical presentation Pain, and segmental symptoms where there is constriction of the neural foramina (see Prolapse) • Progressive as in osteoarthritis.

• Therapeutic options Lumbago is treated with analgesics and infiltration of pain relieving drugs where indicated. Physical therapy • Radicular symptoms may require foraminotomy, posterior spacers, or spinal fusion.

111

Fig.3.22 Conventional oblique radiographs of the lumbar spine. Marked spondylarthritis with joint space narrowing. subchondral sclerosis, and marginal osteophytes.

112

Facet joint Degeneration a

Fig. 3.23

a, b

Conventional

A-P and lateral radiographs

the facet joints with significant

thickening

of the cervical

spine. Sclerosis in

and joint space narrowing.

113

Focet joint Degeneration

o

,.a

~ ~

...•

Fig.3.24 Conventional oblique radiograph of the cervical spine. Marked foraminal stenosis at (3-(4 in spondylarthritis .

~. o ;;;. o

~ Ol

Fig.3.25 a of L3 (axial. bone window). Markedly irregular demarcated facet joints with subchondral sclerosis, joint space narrowing. and marginal osteophytes consistent with spondylarthritis.

114

Facet Joint Degeneration

b

a

,..

.I , ~

'.

, , .. f, Jd \ I, ."If'

e' , ..'

~,

'

\

'.

,

Fig.3.260-< MR image of the lumbar spine (detail a; axial b; sagittal c; T2). Effusion. subchondral sclerosis. osteophytes. deformation.

Differential Diagnosis Inflammation

-

History Erosion Other changes typical of inflammation Possibly synovitis

or infection

- IT is often better - History

Fracture

Selected

References

Bohndorf

K. Imhof H. Radiologische

Diagnostik

der Knochen

und Gelenke.

2nd ed. Stutt-

gart: Thieme 2006 Resnick. D. Niwayama

G (eds.). Diagnosis

of Bone and Joint Disorders.

3rd ed. Philadel-

phia: Saunders 1995 Tournade A. patay Z. Krupa P. Tajahmady T, Millon S. Braun M. A comparative study of the anatomical. radiological and therapeutic features of the lumbar facet joints. Neuro-

radiology 1992; 34: 257 Vahlensieck M. Reiser M. MRT des Bewegungsapparares.

3rd ed. Stuttgart: Thieme 2006

115

Definition ~ Epidemiology Occurs in the setting of degenerative spinal disease with increasing age. ~ Etiology, pathophysiology, pathogenesis Proliferation of osteophytes along the posterolateral margins of the cervical disk interspaces • Uncovertebral "spondylosis" • Posttraumatic. Typically there is no disk material along the margins of the disk interspaces in the cervical spine. Loss of disk height leads to local irritation with compression and traction. This stimulates bone remodeling. Subsequent osteoarthritic changes, which are also influenced by scoliosis and asymmetry. Imoging Signs ~ Modality of choice - Conventional A-P.lateral. and oblique radiographs. - CTand/or MRIare indicated for radicular symptoms. ~ Radiographic findings In the cervical spine, the posterolateral vertebral margins appear jagged with proliferation of osteophytes and narrowing of the disk interspaces • Subchondral sclerosis. Deformation. ~ CTfindings Signs of osteoarthritis in a pseudarthrosis with joint space narrowing.

Marginal

osteophytes • Sclerosis. Deformation. ~ MRI findings Degenerative changes in a pseudarthrosis with marginal osteophytes • Joint space narrowing. Bone marrow changes. Edema. rosis • Deformation.

Fatty degeneration.

Scle-

Clinical Aspects ~ Typical presentation Pain especially in rotation.

Narrowing the neural foramina will also produce

segmental symptoms. ~ Therapeutic options In cervical pain syndrome, analgesics. corticoids, and/or infiltration of pain re-

lieving drugs may be indicated. Physical therapy • Manual therapy • Surgery (foraminotomy) may be indicated for radicular symptoms. Differential Diagnosis

............................................................................................

Congenital vertebral deformity Selected References Bohndorf K,Imhof H. RadiologischeDiagnostik der Knochen und Gelenke. 2nd ed. Stuttgart: Thieme 2006 Dihlmann

116

W.Joints and Vertebral Connections. Stuttgart: Thieme 1985

Uncovertebral Osteoarthritis

Fig.3.27 Conventional A-P radiograph. The uncovertebral joints are seen (some vertebral rotation is present due to degenerative abnormal mobility). The margins appear jagged and the joint space narrowed with increased sclerosis in the superior segment (arrow): the uncovertebral joint in the inferior segment (arrow) appears normal.

Fig.3.28 Conventional oblique radiograph. Large osteophytes in the uncovertebral region consistent with uncovertebral "joint osteoarthritis."

Flg.3.29 CT (coronal reconstruction). The uncovertebral "joints" appear thickened and jagged with narrowing of the joint spaces and subchondral sclerosis.

117

Definition

............................................................................................

~ Epidemiology Occurs in the setting of facet joint degeneration with increasing age. Lower lumbar spine' More common in men than women. Peak age 40-60 years. ~ Etiology, pathophysiology, pathogenesis Synovial cyst of the facet joint in spondylarthritis (synovial irritation with effusion) • No synonyms. Degenerative synovial cyst in the setting of spondylarthritis and synovial irritation and synovitis. Imaging

Signs ............................................................................................

~ Modality of choice MRI: Sagittal, axial (STIR,1'2). ~ CTfindings Difficult to detect because of the poor soft tissue contrast. Osteoarthritis of the facet joints is visualized and synovial enhancement is seen with contrast administration • Hemorrhagic contents and calcification are visualized. ~ MRI findings Synovial cyst (epidural posterolateral lesion) is visualized adjacent to the degenerative facet joint • Signal intensity varies according to whether the contents are isointense to nuid, have a high protein content, or are hemorrhagic' The facet synovium may be thickened; enhancement after contrast administration is a

sign of synovitis (- synovialitis). Clinicol Aspects

............................................................................................

~ lYPical presentation Spondylarthritis is often symptomatic'

Lumbago is present. as are segmental

symptoms in the presence of spinal stenosis or narrowed neural foramina •

Symptoms of degenerative spinal disease. ~ Therapeutic options Infiltration of pain relieving drugs may be indicated for lumbago' Radicular symptoms require surgery (cyst removal with laminectomy or hemilaminectomy).

~ Course and Prognosis Typical course of osteoarthritis.

118

Good success rate.

Synovial Cyst

Fig. 3.300, b

MR image of the lumbar spine (sagittal. STIR.T1). Synovial cyst Isointense to fluid with significant compression of the dural sac.

Differential Diagnosis Root conal cyst

- Communicates with the subarachnoid space. isointense to CSF - Root courses within the cyst

Disk herniotion

- Continuous with and often isointense to the disk - Rarely posterolateral - Not always identifiable

Selected References Bohndorf K. Imhof H. Radiologische Diagnostik der Knochen und Gelenke. 2nd ed. Stuttgart: Thieme 2006 Vahlensieck M. Reiser M. MRT des Bewegungsapparates. 3rd ed. Stuttgart: Thieme 2006

119

Definition ............................................................................................ Thickening of the ligamenta flava in excess of 6 mm in the setting of degenerative spinal disease. Often due to muscular insufficiency. Often incipient degenerative spinal or disk disease. Shift in the axis and resulting abnormal stresses place excessive loads on the ligaments. Scoliosis and asymmetry also influence this disorder • Predilection for the lumbar spine. Imaging Signs ............................................................................................ o Modality of choice MRJ:axial, n. o MRI findings Thickening of the ligamenta flava in excess of6 mm. Clinical Aspects ............................................................................................ o Typical presentation Most cases are asymptomatic, although pain may occur. With spinal stenosis there may also be segmental symptoms (see also Spinal Stenosis, p. 126). o Therapeutic options See also Spinal Stenosis, p. 126. Differential Diagnosis ............................................................................................ Ligament ossification

- Ossification of the ligamentum flavum, middle cervical and lower thoracic spine - Rare

Selected References Vahlensieck

fig. 3.31

M. Reiser M. MRT des Bewegungsapparates.

MRimage (axial,T1). Spinal

stenosis with marked

ligamenta flava.

120

thickening

of the

3rd ed. Stuttgart:

Thieme

2006

Definition

............................................................................................ Interspinous pseudarthrosis'

"Kissing spine" • In the setting or increased lordosis,

reactive cartilage and bone formation occurs in the spinous processes.

This in turn

leads to calcifications in the supraspinous and interspinous ligaments, also rarely in the ligamentum flavum • The height or the disk interspaces is orten reduced. In the terminal stage this leads to thickening or the spinous processes. Most commonly occurs in the lumbar spine' In rare cases, the cervical spine may also be arrected.

o

II> lC II>

:::> II>

Cl~ ;;:. II>

o ;;;. o

a. II>

••

Imaging Signs

............................................................................................ • Modality of choice Conventional radiographs with supplementary stress views. • Radiographic findings SuFficient in nearly all cases. A-P and lateral. Additional flexion and extension views may be needed to confirm the diagnosis' Abnormal contact between adjacent spinous processes with increased sclerosis.

• MRI findings - Calcification orthe ligaments (hypointense on TI- and T2-weighted images) - Cystoid ligament degeneration (hyperintense on T2-weighted images). Clinical Aspects

............................................................................................ • Typical presentation Middle-aged and elderly patients complain or chronic lumbago' Symptoms are aggravated by activity requiring prolonged stooped posture (spinal fiexion) • AFrected areas are tender on palpation and painrul when tapped. Very rarely, the discomrort can also radiate to the legs. •. Therapeutic options Physical therapy with muscle strengthening and muscle relaxing exercises. Heat therapy' Ergotherapy' Acute symptoms may require a brier course or analgesics or local infiltration or pain relieving drugs.

121

Baastrup Disease

Fig. 3.320. b Baastrup disease. Conventional radiographs of L2-L4 (A-P and lateral. detail). Thickening of the spinous processes with "kissing spine."

Differential Diagnosis ............................................................................................ Scoliosis

- Severe deviation from normal axis - Peak age from birth to age 20

Trauma

-

Fracture of the spinous process is extremely rare Bony bridging in the fracture region Ossification in the surrounding soft tissue mantle Often accompanied by degenerative disk disease and osteoarthritis in the adjacent joints

Disk herniation

- Sensory deficits or loss of strength in the extremities

Caldum pyrophosphate disease (CPPD)

- Sclerosis occurs only in the ligamenta nava: the interspinous ligaments are not involved

Selected References Josenhans

G. Kreuzschmerzen

bei Dornfortsatzveranderungen:

schen Krankheit. Z Rheumaforsch 1954: 13: 361 Resnick D. Degenerative diseases of the vertebral column.

1:l:l

Eine Studie zur BaastrupRadiology

1985;

156: 3

~~fi?ft!?~

.

• Epidemiology L4 or L5 is involved in 90% of all cases. Spondylolisthesis is usually diagnosed during childhood or adolescence. Pseudospondylolisthesis usually occurs after 40 years of age. Predisposing factors for spondylolisthesis include Marfan syndrome. osteoporosis. osteogenesis imperfecta. hereditary factors. and sport such as wrestling. weight lifting. and soccer. • Etiology, pathophysiology, pathogenesis "Genuine or apparent" vertebral slippage. Spondylolisthesis. - Spondylolisthesis: Anterior subluxation of a vertebra with a defect in the pedicle and/or pars interarticularis. This occurs in the setting of either spondylolysis or pars interarticularis dysplasia (the spinous process is in a normal position whereas the vertebral body is anteriorly displaced). _ Pseudospondylolisthesis:

Anterior subluxation of a vertebra with interruption

of posterior continuity of the spine (i.e.. the entire vertebra is anteriorly displaced). Causes include degenerative disk changes and/or facet joint degeneration.

The Meyerding classification has four grades: 1-4 (displacement of < 25%. < 50%, < 75%,and 100%)(see also Fig.2.35. p. 81). Imaging

Signs

............................................................................................ • Modality of choice Conventional oblique and stress radiographs are sufficient in most cases. CTor MRI may be indicated where extensive clinical symptoms are present (spinal stenosis). • Radiographic findings Anterior displacement of a vertebra relative to the adjacent caudal vertebra. In spondylolysis. a rypical "collar" can be observed on the "Scotty dog" figure on the oblique films. Stress radiographs: Evaluation of stability (degree of maximal anterior and lateral displacement) in flexion, extension. and lateral bending. • CTfindings - Used for detailed evaluation of spondylolysis. as incomplete ring following a fracture or spinal stenosis can be precisely visualized. - Evaluation of degenerative changes causing pseudospondylolisthesis. • MRI findings T1- and T2-weighted images show reduced signal intensity in the pars interarticularis in spondylolisthesis. In pseudospondylolisthesis, findings include degenerative changes (reduced disk height. a hypointense disk, Modic sign, and osteoarthritis of the facet joints). Early spondylolysis: Vertebral arch shows edema with linear interruptions. Spondylolisthesis: Only the vertebral body displaces anteriorly (spinous process remains

in its normal

position).

123

Spondylolisthesis

and Pseudospondylolisthesis

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b fig. 3.33a. b Lateral view of lumbar spine. Spondylolisthesis spondylolisthesis without defect (b).

with defect (a). Pseudo·

fig.3.34a.b Conventional lateral radiograph (a) and MR image (sagittal. T1; b). Spon· dylolisthesis with anterior slippage at LS-S 1, spondylolysis in the vertebral arch of LS.

124

Spondylolisthesis

and Pseudospondylolisthesis

Pseudospondylolisthesis: Entire vertebral displaces anteriorly (including the spinous process) • The spinal canal and/or neural foramina may be narrowed (spinal stenosis) • Lossof fatty tissue around the nerve root. Clinical Aspects

............................................................................................ • Typical presentation Often asymptomatic in younger patients. Chronic back pain that increases with strenuous activity. Higher-grade spondylolisthesis is often also associated with radicular symptoms. gait abnormalities. paresthesias. or signs of spinal stenosis with bladder and rectal dysfunction . • Therapeutic options Grades 1 and 2: Conservative therapy with a corset. restriction of physical activity. and physical therapy. Grades 3 and 4 (also applies to any symptomatic form): Posterolateral fusion or cast treatment. Analgesics may be prescribed for a short period of time when acute symptoms are present.

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Differential Diagnosis Partialfacetectomy ar sclera tic neck af the pars interarticularis Trauma with fracture Past laminectomy Spondylitis

- Can mimic spondylolysis

Selected References Coughlin WF.McMurdo SK.CTdiagnosis of spodylolysis of the axis vertebra. AJR1989: 153: 195 LeeJ-H. Ehara S.Tamakawa Yet al. Spondylolysis of the upper lumbar spine: Radiological

features. Clin Imag 1999:23: 389 Shipley JA. Beukes CA. The nature of the spondylolytic defect: Demonstration of a communicating synovial pseudarthrosis in the pars interarticularis. J Bone and Joint Surg

8r 1998; 80: 662

125

Definition ............................................................................................ Narrowing ofthe spinal canal from all sides due to numerous changes that reinforce each other in the setting of degenerative spinal disease. Spinal stenosis resulting from several components of degenerative spinal disease: - Spondylosis deformans. - Disk displacement. - Osteoarthritis of the facet joints. - Synovial cysts. - Uncovertebral osteoarthritis. - Thickening of the ligamenta flava. - Subsequent abnormal mobility in the spine with degenerative pseudospondylolisthesis, which itself is conducive to the pathology described above. Imoging Signs ............................................................................................ • Modality of choice - Conventional radiographs: A-P,lateral. and stress radiographs. - CT: coronal, axial.

Bony stenosis.

- MRI: coronal, axial, Tl, T2 • Neural structures. • Radiographic findings An initial radiograph will provide an overview of axial deformities and of the severity and distribution of overall pathology. Stress view obtained with patient standing (or sitting). Other stress views (flexion, extension, lateral bending) to quantify degenerative instability. Exclusion of other severe pathology. Stress views are obtained in maximal flexion, extension, and/or lateral bending. Normally the individual vertebrae overlap one another like roof shingles in flexion, while the disk interspaces show uniform anterior expansion in extension.

Look for any segmental blocks, motion in the opposite direction, or vertebral displacement. Motion must invariably progress uniformly, with the angle of motion increasing continuously from C2 to C7. • CTfindings Demonstrates the width of the spinal canal and also the width of the neural fo•

ramina. MRI findings

This modality allows the best evaluation of the overall situation with high soft tissue contrast and good visualization of the neural structures with any secon-

dary radiculopathy or myelopathy. There may be atrophy of the paravertebral musculature. Width of the spinal canal: Interpedicular distance < 16 mm (gray area above this). Transverse diameter < 20-21 mm, L5 < 24 mm, lateral recess < 4-5 mm. It is crucial to obtain a semiquantitative evaluation by comparing findings with unaffected sections. The severity of degenerative spondylolisthesis is graded according to the Meyerding classification (see Spondylolisthesis and Fig.2.35, p. 81).

126

,) .*'; .-, l~

•

Degenerative Spinal Stenosis Fig.3.35 MR image of the lumbar spine (sagittal, T2). Multisegmental stenosis of the spinal canal from posterior osteophytes.

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Fig. 3.360. b MR image of the thoracolumbarspine (a sagittal, b axial; T2). Multisegmental stenosis with maximal severity at l2-L3. where there is median disk protrusion. Hypertrophy of the ligamenta flava, Elongated course of the fibers of the cauda equina. Modic II disk degeneration

with 5chmorl nodes.

127

Degenerative Spinal Stenosis fig.3.37 CTof the cervical spine (coronal reconstruction). Pronounced exten-

sion with marked paradoxical kyphosis (5-0. Posterior pseudospondylolisthesis with spinal stenosis in the presence of severe degenerative disk disease at levels (5-0.

Clinical Aspects ............................................................................................ • Typical presentation Symptoms range from none to severe pain (usually pseudoradicular or segmental pain). Sensory or motor deficits may occur. These will depend on the level of the pathology; cauda equina syndrome involves bladder and rectal dysfunction and "saddle" anesthesia. Simultaneous narrowing of the neural foramina will also produce segmental symptoms (see Herniation). Progressive clinical symptoms suggest primary bone pathology . • Therapeutic options Treatment is conservative, although neurologic symptoms may require surgical decompression (laminectomy, hemilaminectomy, fusion). Diskogenic symptoms often resolve spontaneously, especially in older patients. Differential Diagnosis ............................................................................................ Inflammatory Tumorous conditions

128

- Pannus in rheumatic disorders - Abscess in bacterial infection - Such as ependymoma, bone tumors

Degenerative Spinal Stenosis

Fig. 3.38

Q-C lateral stress radiographs of the cervical spine. Extension with slight kyphosis at levels (4-(6 and moderate degenerative disk disease. The shingle-like anterior displacement is absent in (5-(7, especially in flexion. Functionally fused vertebrae at (5-(6.

129

Selected

References

Bohndorf K. Imhof H. Radiologische gart: Thieme 2006

Diagnostik

der Knochen

und Gelenke. 2nd ed. Stutt-

Dihlmann W.Joints and vertebral connections. Stuttgart: Thieme 1985 Greenspan A. Drthopedic Radiology. cott Williams and Wilkins 2000 MolierT,

ReifE.

Vahlensieck

130

cr-

A Practical

und MRT-Normalbefunde.

Approach.

Stuttgart:

M. Reiser M. MRT des Bewegungsapparates.

3rd ed. Philadelphia:

Thieme

Lippin-

1998

3rd ed. Stuttgart:

Thieme

2006

~e!!':'.i.t!?~

.

• Epidemiology Present in 6-12% of people over 40 years. Thoracic: 100%. cervical: 65-80%. lumbar: 70-90% • Twice as common in men than women. • Etiology, pathophysiology, pathogenesis Etiology: unclear; presumably there is some relation to diabetes mellitus. hypoglycemia. and hyperuricemia. Synonyms: Forestier disease. ankylosing hyperostosis. "Flowing" ossification of the anterior longitudinal ligament • The height of the disk interspaces is normal. The facet joints appear normal. Combined with enthesis ("whiskering") of the iliac crest. ischial tuberosity. and greater trochanter. Imaging Signs ............................................................................................

• Modality of choice Conventional radiographs. • General Broad-based. "nowing" ossifications on the anterior spine. extending across at least four vertebrae. Slight associated degenerative changes. The facet joints and sacroiliac joints are normal! • The disks are largely intact. • Radiographic findings Bone remodeling on the anterior aspect of the vertebral bodies. Rarely occurs in combination with ossified posterior longitudinal ligament (OPLL). • CTfindings Thick ossification anterior to the vertebral bodies. Initially. there is a typical gap between the ossification and the vertebral bodies. Ossification is more pronounced in the right lateral than left lateral region. • MRIfindings Bone marrow present in ossifications.

Spinal stenosis

with ossified posterior

longitudinal ligament. Clinical Aspects

• Typical presentation Restricted mobility. Rarely difficulties swallowing. Usually asymptomatic. •.. Therapeutic options Mostly none. In severe cases with clinical symptoms. surgery with removal of the calcifications.

131

Diffuse Idiopathic Skeletal Hyperostosis

Conventional lateral radiograph of the thoracic spine. "Flowing" hyperostosis along the anterior margins of the vertebrae (. typical DISH).

Fig.3.39

Differential

Fig.3.4O Conventional lateral tomograph of the thoracic spine. "Flowing" anterior hyperostosis; disks are of normal height (- typical DISH).

Diagnosis

............................................................................................

Spondylosis

- Osteophyte formation - Rarely extends over several segments - Additional degenerative signs

Ankylosing spondylitis

- Sacroiliac and facet joints are also involved - Syndesmophytes ("bamboo" sign)

Selected

References

BrossmannJ. (zerny (hr, FreyschmidtJ. Grenzen des Norrnalen und Anfange des Pathologischen in der Radiologie des kindlichen und erwachsenen Skeletts. Stuttgart: Thieme 2001 Resnick D et al. Association of diffuse idiopathic skeletal hyperostosis (DISH). AJR 1978; 131: 1049-1053

132

Definition

............................................................................................ • Epidemiology The disorder affects 0.5-1.0% of the population .• Annual incidence is 12.0-24.5/ 100000 in men and 23.9-54/100 000 in women .• More common in men than in women (1 :2-3). • Etiology, pathophysiology, pathogenesis Chronic systemic disorder affecting mainly the synovial tissue.

Autoimmune

disease. Synonym: chronic polyarthritis (obsolete term) • Mu/rifactaria/: Genetic susceptibility, association with HLA-DR4,environmental factors, Epstein-Barr virus infection, and certain strains of Escherichia cali • Synovitis (. synovialitis), pannus (. fibrovascular scar tissue), erosion, destruction, deformity. Diagnasis: According to the 1987 criteria of the American College of Rheumatology (formerly American Rheumatism Association): - Morning stiffness. - Joint swelling (more than three joints). - Swelling in the wrist, metacarpophalangeal, and proximal interphalangeal joints.

- Symmetrical joint swelling. - Radiologic abnormalities in the hand (swelling, erosion). - Subcutaneous rheumatoid nodules, Imaging Signs ............................................................................................ • Modality of choice Conventional cervical spine radiographs including stress views.

Conventional

radiographs of the peripheral joints of interest in the hands. MRIof the cervical spine including contrast series. paying special attention to the atlantoaxial joint. •. General

Primarily peripheral joints are affected. In the spine. the disorder shows a predilection for the atlantooccipital. atlantoaxial, and facet joints (the latter especially in the cervical spine) • Rarely. unilateral asymmetric sacroiliitis occurs. • Radiographic findings Most important sign: Anterior atlantoaxial subluxation (occurring in 26% of cases), defined as an atlantodental interval in the sagittal plane exceeding 2.5 mm • Lateral atlantoaxial subluxation (occurs in 14%of cases) • It is important to note that subluxation is occasionally detectable only on stress films. Deformities. Blurred cortex, and erosion of the dens and facet joints.

Inflammatory destruc-

tion of the diskovertebral region (rare). • CTfindings CTis superior to conventional radiographs for visualizing bony changes.

Useful

in preoperative diagnostics. prior to surgical stabilization.

133

Rheumatoid Arthritis :;-

Er 3

g

-

Fig. 4.1

Conventional tomogram of

the dens axis (A-P). Erosion of the dens.

Minor erosion in the left lateral atlantoaxial joint (arrow).

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Fig.4.2 Conventional lateral radiograph of the cervical spine (detail. extension view). Atlantodental subluxation due to inflammatory destruction of the ligament complex and capsule.

134

Rheumatoid Arthritis FIg. 4.3

MR image of the cervical spine (sagittal. 12). Atlantodental subluxation. Pannus (arrows).

Fig.4.4

MR image of the cervical

spine

(sagittai. 11. detail). Dens destruction from extensive

pannus tissue (arrows).

135

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3 Q

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fig.4.5 Axial MR image of the atlantodental joint (axial fat-saturated Tlweighted image with contrast). Hypervascularized pannus tissue (arrows). Dens destruction.

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~ MRI findings Shows bony changes and the inflammatory process. Pannus is hypointense on Tl-weighted images, heterogeneous on T2-weighted images. and enhances proportionally to inflammatory activity. Identifies reactive. inflammatory. and stress-related bone marrow edema (hypointense on Tl-weighted images, hyperintense on T2-weighted and STIR images. enhances with contrast administration) • Effusion into the facet joints (hypointense on Tl-weighted images. hyperintense on T2-weighted images. contrast diffusion) • For evaluating spinal canal. spinal cord, and spinal nerves. Early identification of fractures and stress lesions. Clinical Aspects

............................................................................................

~ Typical presentation Peripheral toms.

joint symptoms.

C-reactive protein is elevated. tors. Rheumatoid nodules, ••. Therapeutic options

Back pain.

Morning stiffness.

Rheumatoid

factor is elevated.

Neurologic Hereditary

sympfac-

Physical therapy • Medical therapy: Nonsteroidal antiinflammatory agents, sulfasalazine. methotrexate, corticosteroids, anti-TNF • Surgical treatment to achieve stabilization and/or decompression of the spinal canal.

136

Rheumatoid Arthritis Differential Diagnosis ............................................................................................ Seronegative

spondyloarthropathy

-

Syndesmophytes Squaring of the vertebral bodies Pronounced proliferative component Predilection for thoracic spine, lumbar spine,

and sacroiliac joints Degenerative changes in rhe spine Juvenile rheumatoid arthritis

Infeerion

- Osteophytes.

sclerosis. joint space narrowing

- Cervical subluxation, fused vertebrae. occurs in children (below 18 years) - Symptoms in Still disease also include fever. anemia, and hepatosplenomegaly

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- Predilection for thoracic and lumbar spine - Clinical aspects

Selected References Arnett FC, Edwotzhy SM, Bloch DA. et al. The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum 1988: 31: 315-324 Gabriel SE.The epidemiology of rheumatoid arthritis. Rheum Dis Clin North Am 2001: 27: 269-281 Resnick D. Rheumatoid arthritis. In: Resnick D. ed. Bone and Joint Imaging. 2nd ed. Philadelphia: Saunders 1996: 211-234

137

Definition ............................................................................................ • Epidemiology Anterior atlantoaxial subluxation: 26% of affected people. Lateral atlantoaxial subluxation: 14%of affected people. Pathology mimicking basilar impression: approximately 5.5 %of affected people. • Etiology, pathophysiology, pathogenesis Minor trauma or physiologic stresses on tissue damaged and weakened by inlIammation and poor quality bone. Insuffiaency fracture: Slight trauma or physiologic stresses on poor-quality or osteoporotic bone. Imaging Signs ............................................................................................ • Modality of choice - Conventional radiographs. - CTto evaluate complex fractures and to demonstrate spondylolysis. - MRIto evaluate ligaments. joint capsules, inllammatory tissue, and neurologic symptoms, • Radiographic findings Anterior atlantoaxial subluxation: Atlantodental interval in the sagittal plane exceeding 2.5 mm • Interval of 2.5-4 mm results from compromised transverse ligament. Interval> 4 mm results from other compromised ligaments, capsule, and bone. Lateral atlantoaxial subluxation: Asymmetric width of the lateral joint spaces. Pathology mimicking basilar impression: Apex of the dens >3 mm over the McGregor line. Insuffiaency fracture: Volume loss in the affected vertebra, vertebra plana, wedge-shaped vertebra, fish vertebrae, reduced bone density. Spondylolysis in fractures of the pars interarticularis.

• CTfindings Multislice IT with multi planar reconstructions. Demonstrates fractures and displacement. • MRI findings Visualization of inflammatory tissue: Hypointense on Tl-weighted. heterogeneous on T2-weighted images, enhances with contrast. Permits evaluation of ligaments and capsules. Bone marrow edema: Hypointense on Tl-weighted. hyperintense on T2-weighted and STIRimages, enhances with contrast. Osteoporosis: Strongly hyperintense bone marrow signal on Tl- and T2-weighted images. Tl-weighted images are well suited for demonstrating fractures.

138

Rheumatoid Arthritis-Chronic Trouma S

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fig.4.6 Conventional A-P radiograph of the atlantoaxial joint. lateral atlantoaxial dislocation with inflammatory erosive changes in the left lateral region in rheu· matoid arthritis.

fig.4.7 Conventional lateral radiograph of the cervical spine (detail). Normal atlantodental

interval.

Fig.4.8 Conventional lateral radiograph of the cervical spine in flexion (detail). Widened atlantodental interval in rheumatoid arthritis.

139

Rheumatoid Arthritis-chranic

Trauma

fig.4.9 MR image of the cervical spine (sagittal. Tl). Compression fracture of vertebra T6. osteoporotic fish vertebra T3. Degenerative changes in the spine.

fig.4.10 MR image of the cervical and upper thoracic spine (sagittal. T2). Insufficiency fracture of vertebra T6 with multisegmental loss of vertebral height in osteoporosis (Tl- and T2-weighted images. markedly hyperintense bone marrow signal). Patient with rheumatoid arthritis on long-term corticoid therapy. Pannus around the dens.

Clinical Aspects ............................................................................................ ~ Typical presentation Usually asymptomatic or with only minor symptoms. Neurologic deficits are occasionally present. ~ Therapeutic options Depend on the symptoms. Conservative or surgical (stabiiization. decompression where indicated) • Management of osteoporosis.

Differential Diagnosis

............................................................................................

Traumatic subluxation

Selected

- No inflammatory or pannus

pathology

such as erosion

References

Freyschmidt J. Rheumatoide Arthritis. In: Freyschmidt J. Skeletterkrankungen. Klinischradiologische Diagnose und Differenzialdiagnose. Berlin: Springer 1997: 669-685

140

Definition ............................................................................................ ~ Epidemiology Approximately 7% of patients with psoriasis develop arthropathy; spinal involvement usually occurs only in HLA-B27-positive patients. In 15-30%.joint pathology develops even decades before skin manifestations. Predilection for the hands and feet. The sacroiliac joints and spine (especially the thoracic and lumbar spine) are involved in up to 50% of cases. ~ Etiology, pathophysiology, pathogenesis Erosive destructive seronegative polyarthritis with proliferation in bone. Imaging Signs

............................................................................................ ~ Modality of choice - Conventional radiographs: These are usually sufficient for the spine and sacroiliacjoints.

- CTand MRI: Where there are neurologic symptoms. complications (trauma. stress lesions). and equivocal findings. ~ Radiographic findings Squaring of the vertebral bodies (anterior spondylitis produces a straight anterior margin). Ossification of the paraspinalligaments and syndesmophytes (ossification of the outer fibers of the annulus fibrosis) • Proliferative osteoarthritis

(especially in the facet joints) • Asymmetric unilateral or bilateral sacroiliitis with destruction. subchondral sclerosis. and ankylosis. ~ CTfindings Multislice CTwith multi planar reconstruction is especially suitable for optimally visualizing destructive and proliferative changes in the facet joints and sacroiliac joints. ~ MRI findings T1-weighted (with and without contrast administration), T2-weighted. and STIR sequences,

sagittal and axial • Demonstrates

active innammatory processes

(synovitis. abnormal bone marrow signal) in the spine and sacroiliac region. Early identification of stress lesions due to the pathologic bone marrow signal (hypointense on TI-weighted images. hyperintense on T2-weighted images. enhancing with contrast) • Identifies vertebral and foraminal stenoses. In up to 38% of cases. radiologic findings are identical to those in rheumatoid arthritis. In up to 30% of cases. radiologic signs of psoriatic spondyloarthropathy coexist with those of rheumatoid arthritis.

141

Psoriatic Spondyloarthropathy

142

Fig.4.11

Conventional A-P radiograph of the thoracolumbar junction. Ossification of the paraspinalligaments (arrows) in a patient with psoriasis.

Fig.4.12

Fig.4.13 Conventional A-P radiograph of the cervical spine (detail). Facetjoint arthritis atC4-C5 (arrows) in a psoriasispatient.

Conventional lateral radiograph of the cervical spine (detail). Facet joint arthritis at C4-CS (arrow) in a patient with psoriasis and spondylolisthesis.

Axial CTof the iumbarspine (detail). Erosive and markedly proliferative arthritis of the facet joints.

Fig.4.14

Psoriotic Spondyloarthropathy S

Clinical Aspects ............................................................................................

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• Typical presentation Begins with joint pain in one or several joints • In up to 85% of cases, there is skin pathology. Sacroiliitis is present with low back pain, especially at night. • Therapeutic options Physical therapy. Medical therapy: NSAIDs. corticosteroids. retinoids, methotrexate, sulfasalazine. ciclosporin. TNF-o blockers.

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·Differential Diagnosis

.

Rheumatoid arthritis

- Predilection for the cervical spine - Erosive and destructive disease components outweigh proliferation - Sacroiliitis is rare (no ankylosis) - Ankylosis is rare

Ankylosing spondylitis

- No skin changes - Symmetric bilateral

Forestier disease (DISH)

- Ossification of the longitudinal - Normal sacroiliac joints

Selected

3 3

sacroiliitis ligaments

References

Freyschmidt J. Psoriasisarrhriris. In: Freyschmidr J. Skeletterkrankungen. Klinisch-radiologische Diagnose und Differenzialdiagnose. Berlin: Springer 1997: 711-718 Stern RS. Psoriasis. Lancet 1997: 350: 349-353 Queiro R, BelzuneguiJ. Gonzalez C. et al. Clinically asymptomatic axial disease in psoriatic spondylarthropathy. A retrospective study. Clin Rheumatol2002: 21: 10-13

143

s

Definition

3 3

• Epidemiology Morbidiry: 0.01 %ofthe population. Occurs more often in men than women (estimated ratio 9: 1) secondary to venereal infection and equally often (1: 1) secon-

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dary to enteric infection.

• Etiology, pathophysiology, pathogenesis Reactive postinfectious seronegative arthritis. Reiter syndrome: Severe arthritis involving the axial skeleton. skin, mucosa. and eyes (uveitis); urethritis. Autoimmune process secondary to gastrointestinal and venereal disease. Associated with HLA-B27(70-90% of cases), Predilection for: - Joints in the lower extremity and heel region, - Sacroiliac joints (in at least 20% of cases). Rarely in the spine (especially in the lower thoracic and lumbar spine). Imoging Signs

............................................................................................

• Modality of choice Conventional radiographs are usually sufficient. Cf and MRIwhen there are negative radiographic and positive clinical findings. Cf for precise evaluation of bony structures. • Radiographic findings No oblique views. Coexisting bony destruction and proliferation. Full radiologic picture of sacroiliitis with destruction. subchondral sclerosis. and ankylo-

sis. often asymmetric. Ossification of the paraspinalligaments • Syndesmophytes (ossification of the peripheral fibers of the annulus fibrosus) • Erosion of the vertebral end plates and narrowing disk interspaces • Rarely atlantoaxial dislocation. Bony ankylosis. • Cffindings High sensitivity for detecting sacroiliac changes. Early detection of erosion in the end plates. • MRI findings Early identification of sacroiliitis: Bone marrow edema and synovitis (hypointense on Tl-weighted images, hyperintense on T2-weighted and STIRimages, enhancing with contrast). Clinicol Aspects

............................................................................................

• Typical presentation Onset up to 60 days after venereal or gastrointestinal infection.

Acute occur-

rence of arthralgia. joint effusion, and inflammation, especially in the lower extremity • Reiter's triad: Arthritis, uveitis. and urethritis. Mucocutaneous symptoms. Conjunctivitis. Occasionally fever. Course is usually self-limiting, occasionally chronic.

144

Reiter Syndrome Conventional A-P radiograph of the lumbar spine. Marginal erosive changes and narrowing of disk space at L2-l3 (arrow) in Reiter syndrome. Coexisting degenerative changes. Flg.4.15

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Conventional A-P radiograph of

the sacroiliac joints. Bilateral symmetric

sacroiliitis with erosions, sclerosis. and joint space narrowing.

145

Reiter Syndrome :;

2i' 3

g

Fig.4.17 MR image of the sacroiliac joints (semiaxial, T2). Bone marrow edema and slight joint effusion in Reiter syndrome.

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• Therapeutic options Physical therapy. Medical therapy: NSAIDs, antibiotics zine.

(tetracyclines),

sulfasala-

Differential Diagnosis ............................................................................................ Ankylosing

spondylitis

Psoriasis Rheumatoid

Selected

- No mucocutaneous

changes

- Joints in the upper and lower extremities - Typical skin changes arthritis

are involved

- Bony destruction without proliferation - Osteoporosis - Appearance and pattern of involvement (hands and feet)

References

Freyschmidt J. Reiter-Syndrom.ln: Freyschmidt). Skeletterkrankungen. Klinisch-radiologische Diagnose und Differenzialdiagnose. Berlin: Springer 1997: 706-711 Hellmann DB. StoneJH. Reiter's syndrome. In: Tierney LM. McPhee S). Papadakis MA, eds. Current Medical Diagnosis and Treatment. Stamford: Appleton & Lange 1999: 827-828 Martel W. Braunstein EM, Borlaza G. et al. Radiologic features of Reiter disease. Radiology 1979: 132: 10 Mohana-80rges AVet al. Monoarticular arthritis. Radiol C1in North Am 2004: 42: 135-149

146

Definition

............................................................................................

:;

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~ Epidemiology Onset: Age 20-40 years. More common in men than women (range 3:1 to 10:1) • Prevalence: 0.2-1.6%. ~ Etiology, pathophysiology, pathogenesis Autoimmune disorder. 96% of affected people are HlJI-B-27 carriers (chromosome 6) • Synonym: Bechterew disease. Chronic inflammatory disorder with predilection for the spine' Seronegative spondyloarthropathy • Affected structures include (a) diskovertebral region. (b) ligamentous insertions. (c) facet joints. (d) costovertebral joints. Peripheral skeletal involvement is seen in 1020% of cases. Associated with: - Ulcerative colitis - Iritis - Aortic insufficiency and atrioventricular conduction disturbance - Pulmonary fibrosis

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Imoging Signs ~ Modality of choice Conventional radiographs in two planes.

Regions of interest include the thora-

cic spine. lumbar spine. and sacroiliac joints. MRIand CT:For early diagnose of sacroiliitis • DO of spondylodiskitis • In difficult cases. With complications such as fracture. spondylolysis. or neurologic symptoms. tJo

General

Destructive and proliferative. Ankylosis. ~ Radiographic findings Squaring of the vertebral bodies: Anterior contour of vertebral body is straight. Biconvex vertebrae: Convex anterior contour of vertebral body • Disk calcifications • Syndesmophytes: Ossification of the peripheral fibers of the annulus fibrosus and between the intervertebral disk and anterior longitudinal ligament • Anterior spondylitis: Spondylitis of the anterior superior and inferior margins of the vertebra. occasionally posterior as well. Sclerosis with or without erosion. Aseptic spondylodiskitis: - Inflammatory type: Destructive granulomatous process in the region of the endplate. - Noninflammatory type: Stress or insufficiency fracture. Erosion on the spinous processes. Arthritis of the facet joints • Ligament calcifications • Full radiologic picture of sacrailiitis: Destruction. subchondral sclerosis, and bony ankylosis. generally bilaterally. ~ CTfindings High sensitivity for identifying sacroiliitis • Involvement of the costovertebral joints. Evaluation of fractures.

147

Ankylosing Spondylitis 5"

21' 3

g

8'

Fig.4.18 Conventional lateral radiograph of the lumbar spine. Anterior vertebral body squaring from periosteal remodeling secondary to anterior osteitis.

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Fig.4.19 Conventional A-P radiograph of the upper lumbar spine (detail). Syndesmophytes.

148

Ankylos;ng Spondylitis Fig. 4.20 MR image of the lumbar spine (sagittal. T2). Syndesmophytes (arrows).

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Fig. 4.21

Conventional lateral radiograph of the thoracic spine (detail). Anterior spondylitis with a predominantly sclerotic

component.

149

Ankylosing Spondylitis :;

3

Fig.4.22 Conventional lateral radiograph of the lumbar spine (detail). Anterior spondylitis with sclerosis and

~

active erosion (arrow).

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Fig.4.23 Conventional lateral radiograph of the lumbar spine. Spondylodiskitis at l4-l5.

150

Ankylosing Spondylitis •

MRI findings Bone marrow edema: Hypointense on TI-weighted. hyperintense on T2-weighted and STIR images. enhances with contrast. Spinal stenosis and neural foramina stenosis. Arachnoiditis with cauda equina syndrome.

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Clinical Aspects

............................................................................................

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• 'Typical presentation Begins with unspecific symptoms in lower thoracic spine. lumbar spine. and sacrum • Low back pain at night. Buttock pain. Stiffness. Peripheral arthritis. Inflammation and pain in musculotendinous insertions. • Therapeutic options Physical therapy. Medicol therapy: NSAIDs. sulfasalazine. methotrexate. antiTNF.

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Differential Diagnosis

............................................................................................ Reiter syndrome

- Arthritis of peripheral joints in the lower extremity - Mucocutaneous changes. uveitis. conjunctivitis - Previous infection

Psoriasis

- Skin changes - Appearance of peripheral - Asymmetric sacroiliitis

DISH. Forestier disease

Selected

- No sacroiliitis - Widespread ossification - Facet joints

arthritis

of the paraspinalligaments

References

Dihlmann W. Spondylitis ankylosans. In: Dihlmann W. Gelenke - Wirbelverbindungen. Stuttgart: Thieme 1987: 591-605 Elyan M. Khan MA. Diagnosing ankylosing spondylitis. J Rheumatol Supp12006: 78: 12-23 Leeb SF et al. Diagnosis and therapy of chronic polyarthritis. Radiologe 1996: 36: 657-662 Levine DS, Forbat SM. Saifuddin A. MRI ofthe axial skeletal manifestations of ankylosing spondylitis. C1in Radio12004; 59: 400-413 Vinson EN, Major NM. MR imaging of ankylosing spondylitis. Semin Musculoskelet Radiol 2003: 7: 103-113

151

:; Definition ............................................................................................

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Up to 20% of all patients with ankylosing spondylitis eventually develop severe disabilities due to progressive ankylosis and ligament ossification.

~

Imaging Signs

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• Modality of choice Conventional radiographs in two planes. MRI and IT where there are complications such as fracture. spondylolysis. or neurologic symptoms. • Radiographic findings Ankylosis of the affected joints. Extensive ligament ossification. "Double railroad track" sign: Ankylosis of the facet joints and calcification of the interspinous and supraspinous ligaments. "Bamboo spine"; Undulating contour from syndesmophytes • Fixed deformity. Atlantoaxial subluxation. • ITfindings Visualization of fractures and pseudarthroses. • MRI findings Stenosis of spinal canal and neural foramina. Cauda equina syndrome resulting from arachnoiditis with formation of diverticula and erosion of the vertebral arches.

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............................................................................................

Clinical Aspects

............................................................................................

• Typical presentation Postural deformity. Restricted mobility. Increased risk of fracture and spondylolysis. •.. Therapeutic options Physical therapy. Treatment is symptomatic and depends on disease activity. Selected References Dihlmann

W. Spondylitis

ankyJosans. In: Dihlmann

W. Gelenke - Wirbelverbindungen.

Stuttgart: Thieme 1987:591-605 HansonJA, Mirza S. Predisposition for spinal fracture in ankylosing spondylitis. AJR2000: 174: 150

ResnickD.AnkylosingSpondylitis. In: ResnickD.ed. Boneand Joint Imaging.2nd ed. Philadelphia: Saunders 1996: 246-264

152

Ankylosing Spondylitis-Ligament

Calcification and Bamboo Spine

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Fig.4.24

Conventional

of the lumbar the facet joints

A-P radiograph

spine (detail). and bridging

phytes ("bamboo"

sign).

Ankylosis syndesmo-

Fig.4.25 of

Conventional

of the lumbar

of the facet joints interspinous

A-P radiograph

spine (detail).

Ankylosis

and ossification

and supraspinous

of the

ligaments.

153

Flg.4.26 Conventional lateral radiograph of the cervical spine. Ossification of the anterior longitudinal ligament with squaring of the vertebral body anteriorly.

Conventional A-P radiograph of the lumbar spine. Ankylosis of the facet joints. "bamboo spine," ossification of the interspinous and supraspinous ligaments. Fig.4.27

154

Ankylosing Spondylitis-Fractures Definition

............................................................................................ • Epidemiology Prevalence of fractures is up to four times higher (up to 17%)in patients with ankylosing spondylitis than in the normal population. Patients with ankylosing spondylitis account for 1.2-1.5% of all patients with spinal cord injuries. Increased risk (up to 8%) of paralytic spinal injury. 75% of all fractures involve the cervical spine. junction.

Second most common fracture site is the thoracolumbar

• Etiology, pathophysiology, pathogenesis Transverse fracture through the vertebral body or disk and the posterior elements (traumatic spondylolysis) and/or dislocation of the facet joints • Rupture of the ligament complex. Often associated with listhesis • Typical injury with minimal trauma • Flexion-distraction injury (82) • Advanced ankylosing spondylitis increases the risk of fracture, mainly due to the altered biomechanics and also due to osteoporosis.

Imaging Signs ............................................................................................ • Modality of choice Conventional radiography is acceptable as the primary imaging modality. CTand MRI (the latter especially where neurologic symptoms are present) are indicated because of their greater sensitivity compared with conventional radiographs . ••. General

Prompt radiologic examination is indicated in patients with ankylosing spondylitis presenting with minimal trauma and/or onset or aggravation of pain.

In

cervical fractures, it is important to exclude injury to the vertebral arteries. • Radiographic findings Focal kyphosis. Abnormal vertical distance between the facet joints and spinous process. Discontinuity in calcified ligaments. Subluxation. Osteopenia and changes due to the underlying disorder can mask fractures. • CTfindings With multi planar reconstruction, multislice CT in particular is significantly better than conventional

radiographs for evaluating fractures.

• MRI findings Evaluation of spinal cord and spinal nerves.

155

Ankylosing Spondylitis-Fractures

3 3

Fig,4.28 MR image of the cervical spine (sagittal, T1), Transverse shear fracture at (6-(7 with anterior subluxation. Rupture of the ligament complex, associated

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vertebral

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fracture,

and compression teoporosis.

facet joint dislocation, ofthe

Complication

spinal cord. Osin ankylosing

spondylitis (syndesmophytes. Andersson lesion at T3- T4 and T7- T8, ligament ossification).

Fig.4.29

MR image

of the cervical

spine

(sagittal, T2), Transverse shear fracture at (4-(5 with anterior subluxation. Rupture of the ligament vertebral

complex,

fracture.

and compression

associated

facet joint dislocation, of the spinal cord. Os-

teoporosis. Complication in ankylosing spondylitis (syndesmophytes, ligament ossification).

156

Ankylosing Spondylitis-Fractures Clinical Aspects ............................................................................................ • Typical presentation Ankylosing spondylitis. Minimal trauma produces symptoms. Sudden onset or aggravation of pain. Minor trauma can cause severe neurologic problems . • Therapeutic options Conservative therapy (cervical collar. halo brace) is not generally indicated. Surgical management aims to achieve: - Reduction of the fracture. Stabilization. - Decompression of the spinal canal where indicated. Selected

References

Hunter T. Durbo HI. Spinal fractures complicating ankylosing spondylitis. Long-term follow-up study. Arthritis Rheum 1983: 26: 751-759 May Pj. Rauneslj. Herdmann j.jonas M. Behandlung der Wirbelsaulenfraktur bei ankylosierender Spondylitis. Unfallchirurg 2002: 105: 165-169. Weinstein PR, Karpmann RR, Gall EP.et al. Spinal cord injury. spinal fracture. and spinal stenosis in ankylosing spondylitis.j Neurosurg 1982: 57: 609-616

157

:;

Definition

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• Epidemiology Peak ages are 10-30 and 50-70 • The lower lumbar spine is the focus of the disorder. • Etiology, pathophysiology, pathogenesis Bacterial spondylitis. spondylodiskitis • Usually caused by Staphylococcus aureus· Primarily hematogenous (venous, arterial). occasionally by extension (as from a retropharyngeal abscess) or postoperatively. Usually begins in the subchondral region. Imoging Signs ............................................................................................ • Modality of choice Early diagnosis: - MRI(Tl. TI. STIR.Tl with contrast). - Scintigraphy. Diagnosis during clinical course:

- Conventional A-P and lateral radiographs. - Scintigraphy. With complications: - MRI(Tl. TI. Tl with contrast). • Radiographic findings Narrowed disk interspace with irregular osteochondral border and increased subchondral sclerosis. Retrolisthesis. • MRI findings Disk appears narrowed. hyperintense on Tl-weighted and STIRsequences. with an irregular osteochondral border and surrounded by a bone marrow edema. Significant enhancement after contrast administration. occasionally in the epidural region. Soft tissue edema, rarely abscess. First signs of healing: - Sclerosis. - Reduced focal uptake on scintigraphy. - Conversion of fatty marrow and reduced enhancement on MRI. C/inlealAspects ............................................................................................ ~ Typical presentation Usually there is marked pain and tenderness to palpation in the affected area. Fever. Erythrocyte sedimentation rate is elevated. • Therapeutic options Long-term antibiotics. Stabilization of the spine (corset. surgery). Surgical removal of abscess where indicated.

158

Acute Bacterial Spondylitis Fig.4.30 MR image of the lumbar spine (sagittal. T2). Subchondral hyperintensity (edema) at L2-L3 with a fine halo (sclerosis. fibrosis). There is partial destruction of the cortex (superior and inferior endplates). Disk height is reduced and there are abnormal changes in the nucleus pulposus (hypointense longitudinal ligament cannot be differentiated; 1-2 weeks before onset of clinical symptoms).

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Fig. 4.31 Bone scan of L2-L3 (detail). Abnormal focal uptake in the subchondral region at L2-L3. disk narrowing with increased focal uptake. Typical picture of spondylodiskitis (1-2 weeks after onset of clinical symptoms) .

•. Course and prognosis With early treatment. the prognosis is very good. 25% of cases become chronic. Complicotions: Abscess. sequestration. Late complications ("healing"): Scoliosis. kyphosis. fused vertebrae.

159

Acute Bacterial Spondylitis :;

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Conventional lateral radiograph of the lumbar spine. Discrete disk narrowing at L2-L3 (6-8 weeks after onset of clinical symptoms) .

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Differential

Diagnosis

Specific spondylitis

- History - Clinical symptoms are usually less severe. less disk involvement. extensive abscesses. softtissue swelling, calcification

Vertebra/fracture

- Osteoporosis. trauma - Contrast images: no inflammation

or abscesses

Metastasis

- Changes in vertebral body; disk is not usually involved - History of underlying malignant disorder - Diffusion sequence (reduced diffusion)

Epidural abscess

- History - Distributed

over several segments

- Vertebtal body and disk ate not the focus of the disorder 160

Acute Bacterial Spondylitis

Fig. 4.330. b eroinferior

Conventional

marginal

tional A-P tomography

lateral radiograph

sclerosis of vertebra (b). Narrowing

(a). Circumscribed

l3 with narrowing

osteolysis

with post-

of the l3-L4 disk. (onven·

of the 1.4-1.5 disk with significant

subchondral

sclerosis and irregular osteolysis. Typical findings in chronic spondylodiskitis. The sclerosis is an initial sign of healing.

Selected

References

Dagirmanjian A. et al. MR of vertebral osteomyelitis revisited. AJR1996: 167: 1539-1543 ImhofH, Kramer J. Rand T, Trattnig S. Knochenentzi.indungen (einschlieBlich Spondylitis). Orthopade 1994: 23: 323 Tali IT. Spinal inlections. European Journal 01 Radiology Vahlensieck M. Reiser M. MRT des Bewegungsapparates. Vorbeck

F. Morscher

M. Ba-Ssaiamah

A. Imhof

2004: 50: 120-133 3rd ed. Stuttgart: Thieme

H. Inlektiose

Spondylitis

2006

beim Erwachse-

nen. Radiologe 1996: 36: 795

161

Acute Bacterial Spondylitis :;

5' 3 ~

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MR image of the lumbar spine (sagittal. STIR).The image shows destruction of the lS-Sl disk. The subchondral regions of the adjacent vertebral bodies are also affected. Flg.4.34

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Flg.4.35 MR image of the lumbar spine (sagittal, T1). Vertebral and disk destruction (hypointensity).

162

Acute Bacterial Spondylitis Fig.4.36 MR image of the lumbar spine (sagittal. T1 with contrast). Enhancement of the inflammatory tissue. This is not an abscess.

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Fig.4.37 MR image of the lumbar spine (sagittal. T1 with contrast). The image shows complete destruction of the L4-L5 disk. An area of subchondral inflammation is present. Anterior paravertebral soft tissue swelling (inflammation).

163

Acute Bacterial Spondylitis

5'

:;

Fig.4.38 Conventional A-P radiograph. The Tll- Tl2 and Tl2-Ll disk interspaces

3

are narrowed with irregular margins, in-

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dicating sclerosis with pronounced bridging osteophytes. Chronic (healed) spondylitis.

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Fig. 4.390, b MR image of the lower thoracic spine (coronal. axial. STIR, Tl with contrast). Paravertebral soft tissue swelling at T9- TlO with formation of a paravertebral abscess. Intervertebral disks T9 and TlO are hyperintense (- edema).

164

Fig.4.4O CT of vertebra T12 (axial). Sequestrum in the vertebral body. The vertebral body and parts of the vertebral arch are abnormally dense. Marked soft tissue swelling.

165

Definition

............................................................................................

~ Epidemiology Peak incidence is at 20-40 years. Spinal involvement is present in only 1%of patients with tuberculosis, usually at the thoracolumbar junction. 10%of the patients with spinal tuberculosis also have lung involvement. ~ Etiology, pathophysiology, pathogenesis Tuberculous infestation of the spine. Tuberculous spondylitis or Pon disease; kyphosis in this disease is known as Pott's curvature. Fungi (Aspergillus) • Pseudotuberculous spondylitis. Immunosuppressed patients are at risk. Typical findings: - Multisegmental involvement. - Soft tissue tumor.

- Calcification in 30% of cases. Imoging Signs

............................................................................................

~ Modality of choice Early diagnosis: - MRI. - Scintigraphy. Diagnosis during clinical course (late diagnosis): - Conventional radiographs. - MRI(with complications). ~ Radiographic findings Inflammatory destruction of bone, diffuse sclerosis (visible on radiographs later than on cross-sectional images) • Disk space may be narrowed with an irregular margin. Secondary spinal deformities (gibbus) and fused vertebrae are well visualized on plain films. ~ CTfindings CTalso shows typical signs of osteomyelitis with bony destruction; these may occur first in the anterior portion of the vertebral body. Sequestra are well visualized as are typical calcifications of the paravertebral abscesses. ~ MRl findings Always obtain contrast images. Typical inflammatory signal in the vertebral body (osteomyelitis)-hyperintense on STIRimages, hypointense on Tl-weighted images, significantly enhancing, often at the periphery with a sequestrum or necrosis in the center. There may be anterior involvement (anterior spondylitis) • Several vertebral bodies may be affected with dissemination along the posterior longitudinal ligament, possibly sparing the disks. Disk involvement appears as an inhomogeneously enhancing disk, hyperintense on STIRand T2weighted images, with irregular margins. Soft tissue abscesses typically occur in the psoas or epidural regions, appearing hyperintense on STIRand T2-weighted images and hypointense on Tl-weighted images, with significant marginal enhancement.

166

Tuberculous Spondylitis

Frequency distribution of pyogenic (bacterial) spondylitis

o

2

4 6

Frequency distribution of tuberculous spondylitis

2 3

8 10 12 14 16 18 20 Number of cases

4

5

6

7 8

Number

9 10 of cases

4.41 a, b Frequencydistribution of pyogenic (bacterial) spondylitis (a) and tuberculous spondylitis (b).

Fig.

Clinical Aspects ~ Typical presentation Chronic lumbago. occasionally with kyphosis.

Neurologic deficits may be pres-

ent • Subfebrile • There may be a history of residence in an endemic area.

~ Therapeutic options Abscess drainage.

Long-term antibiotics.

Stabilization

surgery). ~ Course and prognosis With prompt treatment. the prognosis is good.

of the spine (corset,

Neurologic deficits may persist.

167

Tuberculous Spondylitis

fig. 4.420, b Conventional A-P radiograph (a) and conventional tomogram (b) of the thoracic spine. Narrowing of the disk. right lateral subchondral osteolysis. fine marginal sclerosis. significant soft tissue swelling spreading to T7 and no. Reactive osteophytes.

168

Tuberculous Spondylitis

Fig. 4.430. b

MR image of the lumbar spine (sagittal. STIRlaJ. T2 IbJ). Posterainferior hyperintensity in L3 and posterior hyperintensity in L4. Disk is partially hyperintense with reduced height.

Differential Diagnosis ............................................................................................ Bacterial spondylitis

-

Vertebral fractute

- Osteoporosis. trauma - Contrast images: no inflammation or abscesses - Changes in vertebral body; disk is not usually involved

Metastasis

History Peak ages 10-30 and 50-70 years Predilection for the lower lumbar spine Spondylodiskitis

- No paravertebral abscesses - History of underlying malignant disorder - Diffusion sequence (reduced diffusion)

Epidural abscess Fungal infection

-

History Distributed over several segments Vertebral body and disk are not the focus of the disorder History Indistinguishable on imaging studies

169

Tuberculous Spondylitis

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Flg.4.44a,b MR image of the lumbar spine (sagittal. T1 [al. T1 with contrast [bl). L3 appears hypointense with an enhancing halo after IV contrast administration (edema with abscess and granulation tissue). Posterior soft tissue swelling spreading to l4.

Selected

References

Bohndorf K. Imhof H. Radiologische gart: Thieme 2006 Tali IT. Spinal infections. Vahlensieck

170

Diagnostik

European Joumal

der Knochen

of Radiology

M. Reiser M. MRT des Bewegungsapparates.

und Gelenke. 2nd ed. Stutt-

2004: 50: 120-133 3rd ed. Stuttgart:

Thieme

2006

Tuberculous Spondylitis

Fig. 4.45 a. b MR image of L3 (axial. Tl with fat saturation and contrast). The area of liquefaction has broken through the cortex posteriorly (with spread along the posterior longitudinal ligament) and in the left lateral region. Large psoas abscesses are present.

171

Definition

............................................................................................

~ Epidemiology More common in men than in women • Highest incidence is at age 50-60 years. Most common pathogens: Staphylococcus aureus. streptococci, Escherichia coli, Pseudomonas; less often anaerobes. mycobacteria. and fungi. ~ Etiology. pathophysiology. pathogenesis Accumulation of pus between the dura mater of the spinal cord and the vertebral periosteum. Hematogenous dissemination (occurring in 60% of cases): Skin and soft tissue infection, infectious endocarditis. pneumonia, urogenital tract infec-

tion • By extension: vertebral osteomyelitis, psoas abscess. paraspinal abscess, trauma. Iatrogenic: lumbar puncture. epidural anesthesia, postoperatively. Imaging Signs

............................................................................................

~ Modality of choice MRI: - Sagittal: n, n, STIR(bone), n with contrast and fat saturation. - Axial: n with contrast and fat saturation. - Coronal (one sequence): Visualization of the paraspinal extension (psoas major). Conventional radiographs: - To demonstrate associated osteomyelitis. ~ CTfindings Used where MRIiscontraindicated • Fluidaccumulation in theepidural space. CT myelography is sensitive but invasive • CT-guided biopsy to identify the pathogen. ~ MR( findings Epidural mass compressing the spinal cord and displacing the dura mater. more often anterior than posterior. May spread through the neural foramina to cause abscess in the psoas major. Signal alteration in the adjacent vertebral bodies and disks with simultaneous spondylodiskitis. Tl: - Hypointense mass, contrast improves demarcation of the abscess membrane.

n: - Homogeneously hyperintense to spinal cord and isointense to CSF. OWl: - Hyperintense signal with corresponding hypointensity on the apparent diffusion coefficient (AOC)evaluation image. Clinical Aspects ~ Typical presentation Back pain. radicular pain. Weakness in the legs. Sphincter dysfunction • Fever. ~ Therapeutic options Surgical decompression via laminectomy and drainage • Systemic antibiotic therapy. 172

Epidural Abscess Recurrence of pain with elevated inflammatory markers (generalized sepsis) after spondylodiskitis. MR image of the lumbar spine (sagittal, T2). Biconvex epidural mass at the level of vertebra L3. The mass is homogeneously hyperintense and demarcated from the spinal cord by a hypointense membrane. Hyperintense in· tervertebral disks at levels L2-L3 through L4-L5. Fig.4.46

fig.4.47 MR image of L3 (axial, T2). The lesion has spread through the left neural foramen, with abscess formation in the left psoas major.

173

Epidural Abscess

2r

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Fig.4.48 MRimage of L3(axial.Tl with contrast and fat saturation). Psoas major

3

abscess and epidural abscess.

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•. Course and prognosis Mortality 5-10%. Neurologic status at the time of the diagnosis is an important prognostic factor. Differential

Diagnosis

............................................................................................

Epidural hemotomo

Vertebral body osteomyelitis Spondylodiskitis Disk herniation

Guillain-Barre (postinfectious

syndrome polyneuropathy)

-

History (trauma. anticoagulation) Acute onset of clinical symptoms Inflammatory markers Limited to the bone Intervertebral disk is involved Signal differs on Tl- and T2-weighted images Pathology limited to one segment No enhancement (except sequestra) No mass effect

Selected References Joshi SM et al. Spinal epidural abscess: a diagnostic challenge. Br J Neurosurg 2003;

17:

160-163 Nussbaum ES et al. Spinal epidural abscess: a report of 40 cases and review. Surg Neural

1992; 38:225-231 Ruiz A et al. MR imaging of infections of the cervical spine. Magn Reson Imaging Clin N

Am. 2000; 8: 561-80

174

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.

Innammatory disorders of the spinal cord and spinal canal of different etiologies. characterized by granuloma formation. ~ Selected clinical conditions Sarcoidosis: Neurologic symptoms occur in 5% of cases. Spinal manifestation is rare. most often between 30 and 40 years. Most often in the cervical spine (> 50%) and thoracic spine « 40%). Wegener granulomatosis: Neurologic involvement is present in 30-50% of cases. Tuberculosis: Neurologic involvement is usually cerebral. rarely spinal • More common in immunocompromised persons (elderly people. children. and patients with HIVor diabetes). Imaging

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Signs

............................................................................................ ~ Modality of choice MRI:

- Sagittal: n. T2. n with contrast. - Axial: Tl with contrast. T2. - Study should include the cerebrum. C5Fexamination: - CN5 sarcoidosis: Pleocytosis. elevated protein content. elevated IgG. and elevated ACE(nonspecific). - Wegener granulomatosis: Pleocytosis. elevated protein content. elevated IgG ("sterile meningitis:' nonspecific). - Tuberculosis: Pleocytosis. elevated protein content. depressed glucose content; PCRidentifies the pathogen. Biopsy: - Granulomas

are seen.

- Wegener granulomatosis: c-ANCAis detected. - Tuberculosis: PCRidentifies the pathogen. ~ Conventional radiographs and CTfindings Associated bony changes are seen. Tuberculous spondy/adiskitis: Destruction of the vertebral body. often multisegmental • Sarcoidosis: Nodular pattern of bony sclerosis in the axial skeleton (nonspecific). lytic and cystic changes in the phalanges and metacarpals (arthritis). ~ MRI findings Leptomeningitis: - linear enhancement after contrast administration. along the spinal cord. nerve roots. and cauda equina.

- Epidural granulomas and tuberculomas. - Enhancing nodular or plaquelike dural deposits.

175

Granulomatous Inflammations :;

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of the Spinal Cord

This patient with known Wegener granulomatosis since several years developed gait disturbances and sensory

Fig.4.49

deficits at various levels in the past few

weeks. MR image of the cervical spine (sagittal. T2). Numerous indistinct hyperintense signal alterations in the spinal cord.

01

Patient with known sarcoidosis. on cortisone therapy, complaining of headache in the past few weeks. NeuroFig.4.50

logic examination

suggests involvement

of long pathways. MR image of the cervical spine (sagittal. Tl with contrast). An enhancing spinal cord lesion is seen at (1-(2, as are two lesions in the caudal portion of the pons (cerebral involvement was present in the underlying disorder). Caution: With cortisone therapy there is usually no meningeal enhancement.

176

Granulomatous Inflammations of the Spinal Cord Intramedullary granulomas and tuberculomas: - T1: Isointense or hypointense. - T2: Isointense. hypointense. or hyperintense. - Nodular or ring enhancement. - Perifocal edema (hyperintense on T2-weighted Tuberculous spondylodiskitis (p. 166)

images).

Clinical Aspects ............................................................................................ • Typical presentation Back pain. Fever. Cauda equina syndrome. and tetra paresis .

Weakness in the legs.

Paraparesis

•.. Therapeutic options Wegener granulomatosis: - High dose cyclophosphamide therapy (alternatively: azathioprine. trexate). - Usually remits but often recurs. Tuberculosis: - Tuberculostatic agents. - Microsurgical resection of intramedullary tuberculomas. Sarcoidosis: - Corticosteroids, usually over several months. - Recurrence is possible.

metho-

Differential Diagnosis

..........................................................................................•. - History - In metastatic leptomeningeal malignancies. the leptomeningeal thickening is more often nodular and irregular.

Lepromeningeal

metastases

- History: postoperative condition. trauma. infection - No intramedullary involvement

Aracl1naiditis Intramedullary

tumors

Multiple sclerosis

Acute transverse myelitis Selected References Lexa FJet al. MR of sarcoidosis in the head and spine: spectrum of maniFestations and ra-

diographic response to steroid therapy. AJNRAm J Neuroradiol1994: 15: 973-982 Moorthy Set al. Spectrum of MR imaging findings in spinal tuberculosis. AJRAm J Roentgeno12002: 179: 979-983 Nishino H et al. Neurological

involvement

in Wegener's granulomatosis:

324 consecutive patients at the Mayo Clinic. Ann Neuro11993;

an analysis of

33: 4-9

177

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Definition ............................................................................................

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~ Epidemiology Incidence is increasing due to the increasing number of immunocompromised

patients. ~ Etiology, pathophysiology, pathogenesis

Innammatory disorder of meninges and subarachnoid space • Innammation with fibrinous exudate.

Pathogenesis: - Postoperative and posttraumatic. - Infectious (bacteria. viruses. fungi. parasites). - Intrathecal application of oil-containing contrast agents (no longer permitted). anesthetics. antibiotics. and steroids. - Intraspinal hemorrhage. Complications: Syringomyelia. spinal arachnoid cysts. arachnoiditis ossificans. Imoging Signs ~ Modality of choice

MRI: - Sagittal (Tl. 12. STIR). - Axial (12). - Sagittal and axial (Tl-weighted) contrast sequences with fat suppression. ~ CTfindings

cr myelography (where MRIis contraindicated): - Irregular accumulation of contrast agent around thickened nerve roots. - Contrast filling defects from granulation tissue. ~ MRI findings

Types: - Type I: Adhesions form conglomerates around nerve roots. - Type II: "Empty thecal sac": The fibers of the cauda equina adhere to the dural sac. creating the impression of an "empty" dural sac on axial images. - Type III: Soft tissue mass in the dural sac is seen in the final stage of the inflammation

process.

Tl: - CSFsignal is increased so that the outer contour of the spinal cord is no longer clearly demarcated. - Usually the meninges and fibers of the cauda equina show homogeneous linear enhancement,

rarely nodular enhancement.

- Diffuse intradural enhancement is seen where the dural sac is filled with innammatory soft tissue. 12: - Thickened nerve roots with adhesions. - Subarachnoid space obliterated by granulation tissue. - Leptomeningeal adhesions.

178

Arachnoiditis Fig. 4.51 Several months after surgery for a herniated disk at L4-LS the patient complained of increasing pain in both legs and then urine retention. Clinical examination revealed "saddle" anesthesia and residual urine. Elevated inflammatory markers. MR image of the lumbar spine (sagittal, T2). Cauda equina fibers cannot be distinguished; some edema is present in vertebrae LS-Sl.

MR image of the lumbar spine (sagittal, T1 with contrast). The thickened cauda equina fibers and L4-LS disk are enhanced, early spondylodiskitis at LS-Sl.

Flg.4.52

179

Arachnoiditis S

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Flg.4.53

MR image of L4 (axial, T2),

The cauda equina fibers are adherent

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MR image of L4 (axial. T2).

Normal pattern of cauda equina fibers.

180

to

the dural sac, creating the impressionof an "empty" dural sac (type II).

Arachnoiditis Clinical Aspects ............................................................................................ • Typical presentation Chronic low back pain' Paresis from tethering and/or compression of the spinal cord. Legweakness. Neurogenic bladder and bowel dysfunction. • Therapeutic options Symptomatic medical treatment. Surgical lysis of adhesions.

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Differential Diagnosis ............................................................................................ Leptomeningeal

metastases

'" ~

_ Enhancement is usually more intense in metastatic leptomeningeal malignancies _ Leptomeningeal thickening is more often nodular. irregular.

and asymmetric

- Not always clearly distinguishable from benign arachnoiditis on MRI - History is crucial to diagnosis Intradural tumor

- History - Tumor usually shows more pronounced

Sarcaidosis

_ Enhancing leplOmeningeallesion usually accompanied by enhancing intramedullary focal lesions - Bony changes in the vertebral bodies

enhancement

Selected References Fitt GJet .11.Postoperative arachnoiditis diagnosed by high resolution fast spin-echo MRI

of the lumbar spine. Neuroradiology 1995: 37: 139-145 Ross JS et al. MR imaging of lumbar arachnoiditis. AJRAm J Roentgenol \987: \49: 1025-1032 Struffert T et .11.Lumbar arachnoiditis as differential chronic spinal symptoms diagnosis.

Radiologe2001: 4\: 987-992

181

Definition ............................................................................................ • Epidemiology Bimodal age distribution with peaks at 10-20 and 30-40 years. Predilection for the cervical and thoracic spine . • Etiology, pathophysiology, pathogenesis Clinical syndrome characterized by dysfunction of motor, sensory, and autonomous nerve pathways due to an acute focal spinal cord innammation • Diagnostic criteria: MRIdemonstrates an enhancing lesion and CSFexamination reveals pleocytosis or elevated IgG. Causes: - ADEM:Acute innammation of the brain and spinal cord; postinfectious, postvaccinal. or sporadic.

- Parainfectious: Viral (herpes simplex. herpes zoster. cytomegalovirus, enteroviruses, Epstein-Barr virus, HIV, innuenza, rabies). bacterial (mycoplasmas, syphilis, borreliosis, tuberculosis). - Systemic disorders: Systemic lupus erythematosus. Sjogren syndrome. sarcoidosis. - Multiple sclerosis. - Paraneoplastic syndrome. - Vascular causes (arteriovenous malformation. vasculitis. spinal thrombosis). - Radiation myelopathy. - Idiopathic. - Atopic. Imoging Signs ............................................................................................ • Modality of choice Acute indication for MRI: - Sagittal: STIR,T2, Tl (with and without contrast). - Axial: n. T1 with contrast. CSFexamination: - Oligoclonal bands. PCR,lgG index, antibodies (mycoplasmas. Borrelia). - Serologic tests according to clinical findings. CT myelography: - Where MRI is not feasible or available. (Caution: Spinal puncture can cause spinal cord swelling.) • MRI findings General: - Slight to significant expansion of the spinal cord. For this reason, imaging studies must be done prior to spinal puncture.

- Lesion extends over more than two-thirds of the cross-sectional area of the spinal cord. - Can extend across several spinal segments (prognosis is poor where more than 10 segments are involved). 182

Acute Transverse Myelitis Flg.4.55

This patient reported weakness

in the arm and leg. increasing over the course of a single day and more pronounced on the right side. Neurologic

status included loss of right corneal reflex and crescentic sensory deficit in the face. MR image of the cervical T2). Intramedullary alteration

spine (sagittal,

hyperintense

signal

at the level of (1-C2. where the

spinal cord is distended.

On the axial T2-

:;

"":!> Q

3 3

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o

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weighted sequence. the signal alterations appear more pronounced on the right side.

Flg.4.56 (sagittal,

MR image of the cervical Tl with contrast).

spine

Lesion shows

partial enhancement.

183

Acute Transverse Myelitis :;

5' 3

MRimage of (1 (axial. T1 with contrast). Delayed enhancement of the lesion.

Fig.4.57

3 Q

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o

<;;.

o

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<;1

- Skip lesions are observed. normal areas in the spinal cord between involved segments. TI:

- Inhomogeneous. - Marginal enhancement (inconstant. transient. and often only briefly detectable). - Enhancement is often delayed. so late sequences should be obtained (several Tl-weighted sequences after contrast administration).

n: - Hyperintense central lesion - Isointense area in the center ("central dot sign") - Sharply demarcated. Clinical Aspects ............................................................................................ • Typical presentation The full clinical picture develops within 24 hours in 45% of patients • Almost all patients have weakness in the legs. Bladder dysfunction. Paresthesia. Back pain. radicular pain . • Therapeutic options Acute management: - High-dose intravenous corticosteroid therapy. - Plasmapheresis. - Antibiotics in infectious cases.

184

Acute Transverse Myelitis

Anticoagulation in patients with systemic lupus erythematosus and antiphospholipid antibodies. - Neurosurgical intervention where indicated. Long-term management: - Rehabilitation. - Pain medication. - Muscle relaxants. • Course and prognosis Partial or complete regression of clinical symptoms occurs after 1-3 months. Usually a monophasic disorder. although recurrent manifestation is possible where there is a predisposing underlying disorder. Differential

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Diagnosis

............................................................................................ Disseminated encephalomyelitis

- Asymmetric clinical symptoms with predominantly sensory dysfunction - Oligoclonal bands in CSF(also in ADEM) - Eccentric signal increase in the white

matter

- Lesion involves fewer than two segments: there are multiple lesions - Enhancement within the lesion in acute episodes Spinal infarction

- Predilection for gray matter - Usually anterior. in the area supplied by the anterior spinal artery

Intramedullary rumors (such as astrocytoma)

- Inhomogeneously hyperintense (T2) - Entire cross- section affected - Blood breakdown products (hyperintense anTI-weighted images) - No skip lesions - There may be intense heterogeneous enhancement

Selected References Kerr DA et al. Proposed diagnostic criteria and nosology of acute transverse myelitis. Neurology 2002: 59: 499-505 Kerr DA et al. Immunoparhogenesis of transverse myelitis. Current Opinion In Neurology 2002: 15: 339-347 Uhlenbrock D. Akute Querschnittsmyelitis, In: Uhlenbrock (Hrsg,) MRT der Wirbelsaule und des Spinalkanals. Stuttgart: Thieme 2000

185

:;

"'::!l

Definition

••••••••••••••••••••••••••••••••.•..•••••••••••••••••••••••••••••••••••••••••••••••••.•.....

Q

3 ~

0' ~

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~ Epidemiology Spinal lesions occur in 55-75% of patients with multiple sclerosis. Isolated spinallesions occur in 20% of cases; 67% of these develop in the cervical spine' Age at which lesions occur is variable.

Twice as common in men than in women.

~ Etiology. pathophysiology. pathogenesis Focal demyelination in the spinal cord. MRI findings do not always correlate with clinical symptoms' Histologic findings include Iymphoplasmacytic infiltrates (usually perivenous) and selective demyelination. later gliosis and scarring. Imoging Signs

............................................................................................

~ Modality of choice - Indication for MRI:Tl, T2, STIR(sagittal), T2 (axial) for proved lesions. Contrast administration (double dose, longer delay) is required to evaluate activity of the lesions. - Supplementaty cerebral MRIis indicated with any newly detected spinal multiple sclerosis. - CSFexamination is indicated to confirm the diagnosis (findings include oligoclonal bands). ~ CTfindings CTis not indicated. ~ MRI findings General: - Plaquelike lesions with nodular, ring-shaped, or arched configuration. - Spinal cord involvement is eccentric, especially affecting the posterior and lateral aspects. - Less than 50% of the cross-sectional area of the spinal cord is affected. - Spinal cord is expanded in the acute phase. - Focal or extensive spinal cord atrophy occurs in chronic cases.

n: - Acute: Isointense to slightly hypointense lesions. Lesions shows marked ring to solid enhancement (detectable for 2-8 weeks). - Chronic: Lack of enhancement. Associated spinal cord atrophy.

T2: - Hyperintense lesions. - In an acute episode, there may be a diffuse perifocal signal increase and expansion of the spinal cord due to associated edema.

186

Spinal Multiple Sclerosis Fig.4.58

A 33-year-old

5-week history

woman

of paresthesias

with a and pro-

gressive motor weakness in both extremi· ties. MR image of the middle thoracic spine (sagittal.

T2). A hyperintense

intra-

medullary lesion is seen at the level of T4.

Fig.4.59 MR image of T2 (axial. T2). The intramedullary lesion is located in the right posterolateral region.

187

Spinal Multiple Sclerosis

3

Fig.4.6O MR image of the thoracic spine (sagittal. diffusion-weighted). Here, too. the lesion appears hyper-

~

intense.

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Fig. 4.61

MR image of the thoracic spine (sagittal, T1 with contrast). Enhancing lesion.

188

Spinal Multiple Sclerosis

. -;:,s

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Q

• Typical presentation Sensory deficits. Spastic paresis. Neurogenic bladder and bowel dysfunction. Devic disease (neuromyelitis optical: Bilateral optic neuritis and high paraplegia. Clinical course is episodic with complete or incomplete remission between episodes. • Therapeutic options Glucocorticoids during the episode. Prophylaxis with interferon. copolymer 1, azathioprine.

mitoxantrone

(patients with severe clinical course). low-dose me-

3 3

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thotrexate • Symptomatic medical therapy. Differential Diagnosis

............................................................................................ Astrocytoma

Ependymoma

Acute transverse myelitis

- Usually extends over a longer distance (more than two vertebrae) - Rarely multifocal - Central intramedullary location - Extends over a long distance - Associated cysts - Extends over a longer longitudinal distance than multiple sclerosis, often involves more than 50% of the cross-sectional area of the spinal cord - History (infectious, toxic. autoimmune)

Acute spinal infarction

- Paramedian involvement

Sarcoidosis

less often anterior spinal cord - Enhancing parenchymal lesions and possibly linear leptomeningeal enhancement are also present - When in doubt, biopsy can confirm the diagnosis

Systemic lupus

- Picture of transverse myelitis

of posterior spinal cord.

erythematosus

Selected References Hickman SJ. Miller DH. Imaging of the spine in multiple

sclerosis. Neuroimaging

Clin N

Am. 2000 Nov: 10:689-704

LosseffNAet al. T1 hypointensity of the spinal cord in multiple sclerosis. J Neurol 2001: 248: 517-521 Tartaglino LM et al. Multiple

sclerosis in the spinal cord: MR appearance and correlation

with clinical parameters. Radiology 1995: 195: 725-732

189

Definition

............................................................................................

~ Epidemiology Common (prevalence is 10% of the population) • Primarily affects the thoracic spine.

~ Etiology, pathophysiology, pathogenesis Benign vascular tumor (cavernous, capillary, venous) • Usually an incidental finding (possibly malformation) • Usually limited to the vertebral body. In rare cases, the posterior elements are also involved. Cystic angiomatosis (diffuse skeletal form) • Vertebral collapse can occur as complication • Aggressive (symptomatic) form is rare and characterized by growth, vertebral collapse, lack of fat storage, and an extraosseous component, Imoging Signs

............................................................................................

~ Modality of choice Conventional radiographs. Where clinical symptoms are present: MRI(enhancement, size), CT. ~ General Typical configuration of trabeculae. Typical radiologic picture (conventional radiographs, CT, MRI). ~ Radiographic findings Circumscribed osteolysis (defect) • Thickened, "stranded" trabeculae aligned axially. ~ CTfindings Circumscribed osteolysis (defect) • Thickened, "stranded" trabeculae aligned axially (multiplanar reconstruction) • Fat deposits. ~ MRI findings T1 hyperintensity • Pronounced 1'2 hyperintensity (fat deposit) • Complications (spinal cord or nerve root compression) • Moderate to pronounced enhancement • Aggressive hemangioma is hypointense on Tl-weighted images, hyperintense on 1'2-weighted images. Epidural spread and fracture often present. Clinical Aspects

............................................................................................

~ Typical presentation Clinically occult • Aggressiveform: Localized pain due to vertebral collapse, radiculopathy, myelopathy. ~ Therapeutic options Only the aggressive form requires treatment (vertebroplasty, embolization; radiation therapy) • With suspected compression: Surgical stabilization.

190

Hemangioma Fig. 5.1 Normal clinical findings. CT (axial). Typically thickened trabeculae showing craniocaudal alignment (salt and pepper pattern).

Fig.5.2 Conventional lateral radiograph of the middle thoracic spine (detail). Coarse. stranded cancellous bone structure. Normal-sized vertebrae.

191

Hemangioma Conventional lateral radiograph of the middle thoracic spine (detail). Fig.5.3

Compressed vertebra in hemangioma

with anterior and posterior displacement (spinal stenosis).

Fig.5.4 MR image of the middle thoracic spine (sagittal. detail). Vertebral hemangioma with fatty marrow (markedly hyperintense).

n.

192

Hemangioma Fig.5.5 MR image of the middle thoracic spine (sagittal. 12. detail). Vertebral hemangioma with fatty deposits (markedly hyperintense).

Fig.5.6 MR image of the lumbar spine (sagittal, 12). Circumscribed subchondral hemangioma.

193

Hemangioma Differential Diagnosis ............................................................................................ Metastasis

- T1 hypointensity - Soft tissue component - Pedicles are often involved - Bony destruction

Remnant of the notochord Selected

- Eccentric

References

Baudrez V. Benign vertebral hemangioma: MR-histological correlation. Skeletal Radial 2001:30:442-426 Heyd R. Radiotherapy in vertebral hemangioma. Rontgenpraxis 2001: 53: 208-220 Manning HJ. Symptomatic hemangioma of the spine. Radiology 1951: 56: 58-65 SaT C. Double thoracic vertebral hemangioma causing complete paraplegia. Am J Orthop 2004:33:81-84,57

194

Definition

............................................................................................ • Epidemiology Age 0-30 years. More common in males than females. Occurs in the spine (posterior elements) in 10%of cases. In order of decreasing frequency: femur (50% of cases), tibia, hand and foot, intraarticular sites, • Etiology, pathophysiology, pathogenesis Benign, osteoblastic tumor. Highly vascularized central nidus and significant marginal sclerosis. Classic clinical symptoms include nighttime pain. Responds to salicylates in 50% of cases. Responds to NSAIDs.

i:' 3 o ;;:

Imaging

Signs ............................................................................................

• Modality of choice Conventional radiographs.

a. •.. General

• •

•

•

Central noncalcified nidus (lysis) with reactive marginal sclerosis. Smaller than 1.5cm (> 1.5cm _ osteoblastoma) • Typical/ocation: Vertebral arch, base of the pedicles (posterior half of the vertebra). Radiographic findings Bone sclerosis with a central radiolucency (nidus). afindings Central hypodense nidus, halo of bone sclerosis. Periosteal thickening. Soft tissue tumor may be present. Very rapidly enhancing. MRI findings Nidus is hypointense on n, hyperintense on TI • Sclerosis is hypointense on n and TI. Nuclear medicine (SPEa) Uptake is greatly increased in nidus and increased in sclerotic halo· FDG-PET (highest specificity).

Clinical Aspects

............................................................................................ • Typical presentation Nighttime pain that responds to salicylates in 50% of cases. Painful scoliosis. Muscle atrophy' Focal radicular pain. • Therapeutic options Surgical resection of the nidus. a-guided percutaneous procedure to sclerose the nidus.

195

Osteoid Osteoma

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1f' ' Fig. 5.70, b Nighttime back pain. Slight scoliosis, Pain eliminated with salicylates, A·P radiograph of the thoracolumbar junction (detail; a). Fine sclerosis in the right pedicle of vertebra T12. P-A bone scan (b). Increased uptake on the right in vertebra T12, Fig.5.B CT (axial). Subarticular nidus with slight sclerosis.

196

Osteoid Osteoma

Differential Diagnosis

............................................................................................ Osteoblasroma (> 1.5 an) Stress fracture of the pedicle Osteoblastic metastasis breast carcinoma lymphoma, prostate cardnoma

- Multicystic,

Aneurysmal bone cyst Sclerotic bone islands

Inflammation

- Older patients - Pedicles and/or anterior bodies often involved expansile.

vertebral fluid sign

- No nidus - No clinical symptoms - Normal scintigraphy findings

(Brodie's abscess, sequestrum)

- Slowly enhancing

Tips and Pitfalls

............................................................................................ Orren misdiagnosed

as the MRI resolution

chosen is insufficient

for examining

de-

tails. Selected References Ciani R. CT-guided radio(requency ablation of osteoid osteoma: long-term results. Eur Radio12004: 14: 1203-1208 Lindner NJ.Percutaneous radiofrequency ablation in osteoid osteoma.J BoneJoint Surg Bf 2001:83: 391-396 Ozaki T. Osteoid osteoma and osteoblasroma of the spine: experiences with 22 patients. Clin Orrhop 2002: 397: 394-402

197

Definition

• Epidemiology Age 0-30 years (70% of cases aged 10-30 years) • Occurs in order of decreasing frequency in the cervical spine (40%). lumbar spine (20%), thoracic spine. and sacral region. Sites in order of decreasing frequency include the spine, flat bones (skull, mandible. pelvis). long bones (primarily in the diaphysis). More common in males than females, • Etiology, pathophysiology, pathogenesis Highly vascularized osteoid-forming tumor larger than 1.5em • Benign, expansile, usually osteolytic. Typically occurs in the posterior half of the vertebra, Benign type: Primarily sclerotic. Aggressive type: Osteolytic with a soft tissue component. Fifty percent of all lesions recur; no metastases! Imaging

Signs

• Modality of choice Conventional radiographs. CT.

• General Sharply demarcated oval lytic tumor (50% of cases) with marginal sclerosis. Caution: Soft tissue component, periosteal reaction, and cortical thinning can occur.

• Conventional radiography and CTfindings Expansile, usually sclerosing tumor of the vertebral arch and pedicle. Newly formed bone has a ground-glass structure. • MRI findings Sclerosis hypodense on T1 and T2 • Osteolysis and soft tissue component appear as Tl hypointensities and T2 hyperintensities • Caution: Edema can mimic a malignant tumor and/or inflammation. Marked peri tumoral edema. Clinical Aspects

·.....................................•.....................................................

• Typical presentation Pain that can only be partially alleviated with salicylates or NSAIDs• Painful scoliosis • Focal radicular pain. Muscle atrophy. • Therapeutic options Surgical resection.

198

Embolization.

Osteoblostoma Nighttime pain and increasing scoliosis. Conventional A-P radiograph of the lower lumbar spine. Destruction of the right pedicle and transverse process in vertebra l4.

Fig.5.9

CT of vertebra L4 (axial). Expansile osteolytic lesion (osteoblastoma) surrounded by a fine sclerotic halo.

Flg.5.10

199

Osteoblastoma Differential

Diagnosis

............................................................................................

Osteoid osteoma « 1.5 em) Osteoblastic metastasis breast carcinoma lymphoma, prostate carcinoma Aneurysmal bone cyst

Sclerotic bone islands

Primary bone tumors

- Older patients - Pedicles and/or anterior vertebral body often involved - Destruction instead of expansion - Multicystic, fluid sign: yet they also occur with osteoblastomas - Secondary aneurysmal bone cyst in osteoblastoma - No nidus - No clinical symptoms - Normal scintigraphy findings - Fibrous dysplasia - Histiocytosis X (primarily vertebral body) - Giant cell tumor (10-40 years; primarily vertebral body) - Enchondroma, osteochondroma (popcorn-like matrix calcification) - Osteosarcoma (extremely rare in the spine)

Selected References Chew FS.Cervicalspine osteoblastoma. A]RAm] Roentgeno!.1998: 171: 1244 Schneider M. Destructive osteoblastoma of the cervical spine with complete neurologic recovery.Spinal Cord 2002: 40: 248-252 Sanel B. OsteobJastoma of the lumbar spine as a cause of chronic low back pain. Rheumatollnt 2002; 21: 253-255

200

Definition ............................................................................................ • Epidemiology Primarily 10-30 years of age. More common in females than males. Frequency of osteochondroma in the spine is less than 7% • Predilection for the cervical spine, most often C2 (50% of cases). • Etiology, pathophysiology, pathogenesis Exostosis (solitary or multiple, sessile or peduncular) • Painless and slow-growing • Caution: Irritation of spinal cord, nerve roots, or vascular structures may occur. Rapid growth and a cartilage cap thicker than 1.5cm are signs of malignant transformation

(chondrosarcoma)

• Osteochondromas

can increase in size

during skeletal growth but remain the same size in adults. In growing children, the cartilage cap can be thicker (up to 3 cm) • Caution: This is not a sign of malignancy • Osteochondromas are occasionally associated with systemic disorders: - Pseudohypoparathyroidism. - Pseudopseudohypoparathyroidism. - Myositis ossificans. _ Hereditary multiple exostoses (spinal involvement in approximately 10%of cases). Osteochondromas occasionally occur after radiation therapy (at the margins after a latent period of about 2 years). Imaging

Signs ............................................................................................

• Modality of choice Conventional radiographs. MRI(cartilage cap on cartilage sequence) • CT(continuity with vertebral bone). • General Bony outgrowth arising from vertebra (cortex and cancellous bony are continuous) • Cartilage cap. • Conventional radiography and CTfindings Exostosis with a cartilage cap arising from the vertebra, occasionally pedunculated • Scintigraphy and PETare helpful in evaluating malignant transformation (increased uptake). • MRIfindings Central (mature fatty marrow): Tl and T2 hyperintensity • Cortex: Tl and T2 hypointensity • Cartiloge cap (hyaline cartilage): T1 hyperintensity or hypointensity, T2 hyperintensity. Clinical Aspects ............................................................................................ • Typical presentation Incidental finding, clinically silent. Palpable tumor.

Hoarseness.

Dysphagia.

Restricted mobility. Painless growth. Complications can occur due to secondary irritation of spinal cord. nerve root. or vascular structures. 201

a of vertebra T12 (axial). Cartilaginous exostosis (osteochondro· mal in the right transverse process.

Fig.5.11

Fig.5.12 Conventional A-P radiograph. Circumscribed osteolytic expansion of the L2 vertebral arch with left marginal sclerosis.

202

Osteochondroma Fig.5.13 Conventional lateral tomography. Circumscribed thickened osteolytic expansion of the l2 pedicle. a typical chondroma. not an osteochondroma!

• Therapeutic options Resection (spontaneous remissions are rare) • Recurrences are extremely rare· Multiple exostoses are hereditary; malignant degeneration occurs in 3-5% of cases.

Differential Diagnosis ............................................................................................ Chondrosarcoma

-

Parostealosteosarcoma

- Extremely rare in the spine - Aggressive bone remodeling

Selected

Rapid growth Cartilage cap thicker than 1.5 cm Aggressive Pain 1% of all osteochondromas

References

Aokij. FOG PETofprimary benign and malignant bone tumors: standardized uptake value in 52 lesions. Radiology 2001; 219: 774-777 Gorospe L Radiation-induced osteochondroma of the T4 vertebra causing spinal cord compression. Eur Radio12002; 12: 844-888 Jose Alcaraz Mexia M. Osteochondroma of the thoracic spine and scoliosis. Spine 2001; 26: 1082-1085

203

Definition ............................................................................................ • Epidemiology Peak age 10-30 years. Lesions occur in order of increasing frequency in the thoracic spine. lumbar spine, cervical spine, and sacrum. Typically they involve the posterior elements and spread into the vertebral body. 55-60% of aneurysmal bone cysts are primary lesions. Approximately 45% of all aneurysmal bone cysts are secondary lesions occurring with a giant cell tumor, osteoblastoma, chondroblastoma. fibrous dysplasia. chondromyxofibroma. ete. • Solid aneurysmal bone cysts: Rareform « 5%). • Etiology, pathophysiology, pathogenesis Expansive, thin-walled. multilobulated. blood-filled bone cysts ("egg shells") • Blood or nuid signs, septa. solid components' Cortical thinning. Occasionally associated with preexisting bone pathology (trauma. tumor) • Caution: Underlying malignant process; malignant degeneration may occur. Imaging Signs ............................................................................................ • Modality of choice CT • MRI(in spinal cord compression). ~ General

Expansile. multicystic lesion of the vertebral arch extending into the vertebral body. Blood or nuid sign. • Radiographic findings Expansile. multicystic osteolysis ("egg shells"). • CTfindings Expansile. multi lobulated cysts with a thin sclerotic halo ("egg shell" appearance) • Blood or nuid sign' Compression of the dural sac and nerve roots. Septa and solid components enhance after contrast administration. • MRI findings Hypointensity on n, hyperintensity on T2 and STIRsequences. (Caution: Signal behavior of the blood components varies depending on the breakdown stage) • Blood or nuid sign. Compression of the dural sac and nerve roots. Secondary aneurysmatic

bone cyst: intravenous contrast adminstration; enhancement of

the primary tumor . •.. Nuclear medicine Marginal uptake with ring sign. Clinical Aspects • Typical presentation Pain and scoliosis. Myelopathy. radiculopathy (compression) • Compression fracture. Rapid growth. • Therapeutic options Surgical resection.

feasible.

204

Embolization.

Radiation therapy where resection

is not

Aneurysmal Bane Cyst Fig.5.14

Back pain with scoliosis. CT of

(6 (axial). Extensive expansite osteolysis

and intraspinal soft tissue component.

Fig. 5. J5

CT sagittal reconstruction of the cervical spine. Expansile osteolysis extending across several segments. Partial destruction of vertebra (6.

205

Aneurysmal Bone Cyst

i:' 3

o

~

MR image of the cervical spine (sagittal, T2), Expansile, cystic mass with blood or fluid sign (characteristic but not pathognomonic). Fig.5.16

MR image of (6 (axial, T2). Multicystic mass with blood or fluid sign. Extensive marginal edema.

Fig.5.17

206

Aneurysmal

Bane Cyst

MR image (axial. T1 with contrast). Aneurysmal bone cyst showing marked marginal enhancement and marked enhancement of the surrounding soft tissue . Flg.5.18

••. Course and prognosis Rate of recurrence is about

10-30%.

Differential Diagnosis ............................................................................................ Osteoblastoma. giant cell tumar. fibraus dysplasia Metastases with bleeding

Giant cell tumor Selected

- Blood or fluid sign - Higher peak age. different location - Caution: Aneurysmal bone cysts skip the disk interspaces and can mimic metastases - Manifestation in several bones - Soft tissue component - Compression fracture of the vertebral body - Older peak age. over 30 years

References

de Kleuver M. Aneurysmal bone cyst of the spine: 31 cases and the importance of the surgical approach.] Pediatr Orthop B 1998: 7: 286-292 Murphey

MD. From the archives of the AFIP. Primary tumors of the spine: radiologic

pathologic correlation. Radiographies Erlemann R. Imaging and differential

1996: 16: 1\31-1158

diagnosis of primary bone tumors and tumor-like

lesions of the spine. Eur] Radio12006: 58: 48-67

207

Definition ~ Epidemiology Peak age 20-40 years. Account for approximately 20% of all benign bone tumors and 10%of all primary spinal tumors. Initially malignant giant cell tumors are rare (1-2% of cases) • High recurrence rate (approximately 60%) • Typicol location: Sacrum, vertebral bodies. ~ Etiology, pathophysiology, pathogenesis Osteolytic locally aggressive tumor with osteoclast-like giant cells ("semi-malignant" tumor with lymph node metastases in 1-2% of cases) • Multicentric manifestation (lung metastases) • Osteolysis of the anterior vertebral body; the posterior elements may be involved. Tumor consists of multinucleated giant cells, connective tissue, and a fatty component. Angiogenesis and hemorrhages are common.

Imoging Signs

............................................................................................

~ Modality of choice CT. MRI(spread into spinal canal). ~ General Expansive osteolysis. No matrix calcification.

Slight or absent marginal scle-

rosis • Soft tissue component.

~ Radiographic findings Expansive osteolysis. ~ CTfindings Expansive osteolysis.

Evaluation of articular and neurovascular

involvement.

~ MRI findings Inhomogeneous signal behavior (Tl hypointensity, T2 hyperintensity) • Inhomogeneous, usually marginal enhancement (less often homogeneous) • Evaluation ofthe soft tissue component and involvement of the spinal canal and neurovascular structures • Occasionally blood or nuid sign (less often than with aneurysmal bone cyst). Clinical Aspects

............................................................................................

~ 'JYpical presentation Pathologic fracture. Radicular symptoms. Upper back pain. ~ Therapeutic options Resection and cryotherapy or thermocoagulation. Eventual sequential embolization.

~ Course and prognosis Malignant degeneration can occur secondary to radiation therapy.

208

Giant Cell Tumor Fig.5,19 Conventional radiograph of the sacrum. Large osteolytic defect in the right sacrum (52-55). Histologic diagnosis: Giant cell tumor.

'ii""·· t ~•..J, ~

(

,

};

Fig,5.20 CT (axial). Sharply demarcated solid osteolytic defect in the lateral masses and body of the sacrum. Histologic diagnosis: Giant cell tumor (DO: chordoma. metastasis).

209

Fig. 5.21 MR image of the sacrum (coronal. T2, STIR). Hyperintense, partially lobulated lesion in the left lateral mass (51-53). The tumor extends as far as the sacroiliac joint and has spread to the foramina.

Fig.5.22 MR image of the sacrum (coronal, T1). Hypointense mass in the left lateral mass.

210

Giant Cell Tumor fig.5.23 MR image of the sacrum (axial. T1 with contrast). Tumor shows significant enhancement. Slightly inhomogeneous.

Differential Diagnosis ............................................................................................ Metastasis Aneurysmal bone cyst

- Usually multiple. in older patients - Usually proceeds from the posterior elements (Caution: Blood or fluid signs occur in both entities) - Aneurysmal bone cysts and giant cell tumors can occur together

Selected References BloemjL. Kroon HM. Mulder jD. OoosterhuisjW. Schutte HE.Taconis WK. Taminian AHM. Radiologic Atlas of Bone Tumors. Elsevier 1993 Freyschmidt j. Ostertag H. Hundh G. Knochentumoren. Berlin: Springer 1998

211

Definition

......................................................

~

.

• Epidemiology Age 5-15 years. 10-20% of cases are polyostotic' Occurs in orderof decreasing frequency in the thoracic (50% of cases), lumbar, and cervical spine. • Etiology, pathophysiology, pathogenesis Synonyms: Histiocytosis X. eosinophilic granuloma (bony manifestation) • Rapidly growing, permeative osteolysis primarily occurring in children. Course is invariably benign. Imaging Signs

............................................................................................

• Modality of choice Conventional radiographs' MRJ(multi planar) • CT (spread in bone). • General Osteolytic destruction of the vertebral body; the intervertebral disk is spared. Vertebra plana or wedge-shaped vertebral bodies in children. • Radiographic findings Permeative osteolysis without a sclerotic halo. Central bone fragment (DD: Sequestrum) • Vertebra plana. • CTfindings Osteolysis without a sclerotic halo. Soft tissue component. Homogeneous enhancement.

• MRI findings T1 hypointensity. T2 hyperintensity • Moderate, homogeneous enhancement after contrast administration. Soft tissue component (Caution: spinal stenosis) . •.. Nuclear medicine Unspecific' Up to 30% false negative scans. Clinical Aspects

............................................................................................

•.. Typical presentation Pain. Fever. Chronic disseminated form: Before age 5 years (Hand-SchOller-Christian disease): Skeletal. visceral. and reticuloendothelial manifestation. 10% mortality. Fulminant form: Before age 3 years (Letterer-Siwe disease): Skin, liver, spleen, lymph nodes, skeleton: high mortality. New classification: - Circumscribed Langerhans cell histiocytosis. - Extensive Langerhans cell histiocytosis. • Therapeutic options Spontaneous remission (3 months to 2 years) • Orthopedic support is required. Intralesional steroid injections' Surgical excision is indicated where conservative therapy fails.

212

Langerhans Cell Histiocytosis Fig.5.24 Conventional lateral radiograph of the lumbar spine in an 8-year-old child. Vertebra plana. Disk height is normal.

Fig.5.25 MR image of the thoracic spine (sagittal, Tl). Vertebra plana with hypointensity in vertebra 18.

213

Longerhons Cell Histiocytosis Fig.5.26 MR image of the thoracic spine (sagittal, l2). Vertebra plana at l8. The disks show reactive hyperintensity and thickening ("tram tracking" of the spine). Small anterior soft tissue tumor mass.

Differential Diagnosis ............................................................................................ Ewing sarcoma

- Large soft tissue tumor

Lymphoma

Metastasis Infection

- Later age

Giant cell tumor

- Over 30 years of age

- Spondylodiskitis - Intervertebral disk is also involved

Selected References Azouz EM. Langerhans' cell histiocytosis: involvement. Pediatr Radiol 2004; 28

pathology, imaging and treatment

of skeletal

Raab P.Minimal invasive therapy of localized Langerhans-cell histiocytosis of bone. Z Orthop Ihre Grenzgeb 2000: 138: 140-145

214

~~~i.~?~?c~.c~~~~~~

.

• Growth - Matrix. - Permeative or moth-eaten: Narrow transitional zone or none at all (rapid growth). - Geographic: Broad transitional zone (slow growth). - Smoothly demarcated, sclerotic (minimal or absent growth). • Periosteal reaction (decreasing aggressiveness) - Sunburst. - Hair on end. - "Onion peel" appearance. - Codman triangle. - Double layer cortex. • Morphology (highly aggressive lesion) - Widespread bone marrow edema. - Marked enhancement. - Large soft tissue component.

• Tissue type (benign and malignant) - Bone matrix (osteoid osteoma, osteoblastoma, osteosarcoma). - Cartilage matrix (chondroma, chondroblastoma, chondrosarcoma). - Myxoid matrix (chondromyxofibroma). - Dedifferentiation. - Bone marrow (multiple myeloma and lymphoma). - Unclear (aneurysmal bone cyst, giant cell tumor). • Ages (benign and malignant) - 0-20: Ewing sarcoma. - 10-30: Osteosarcoma, osteoid osteoma, osteoblastoma, aneurysmal bone cyst. - > 30: Lymphoma, giant cell tumor. - > 40: Metastases (above age 40 the most common bony pathology); multiple myeloma.

215

Definition

............................................................................................

~ Epidemiology Primarily affects people over 40 years. Most common spinal neoplasm. Approximately 40% of bone metastases. Often occurs in the thoracic spine. less often in the lumbar spine. ~ Etiology. pathophysiology, pathogenesis Primarily hematogenous metastases (medulla): venous (Batson vertebral plexus). arterial. rarely by extension (neck. bronchus) • Primarily in pedicle and anterior vertebral body (blood supply)' Localization depends on levels of local osteoprotegerin. Osteolytic: Bronchial carcinoma. thyroid carcinoma. renal carcinoma. etc.). Osteoblastic: Prostate carcinoma. breast carcinoma. carcinoid. nasopharyngeal

and bladder malignancies. medulloblastoma. and osteoblastic): Breast carcinoma. bronchial carcinoma. cervical carcinoma. ovarian carcinoma. Occult primary tumor in approximately 20% of cases. Mixed (osteolytic

Imaging Signs

............................................................................................

~ Modality of choice MRI (T1. STIR.T1 with contrast) • Scintigraphy (whole body examination with possible lesions primarily in the skull. ribs. and pelvis) . •.. General - Osteoblastic: Circumscribed sclerosis (irregular). - Osteolytic: Circumscribed void with a sharply demarcated or ill-defined bor-

der. cortical destruction. localized widening of paravertebral soft tissue structures. - Pathologic compression fracture (DO: osteoporosis. trauma. steroid therapy). ~ Radiographic findings Osteolytic metastases are only visible where there is 50% loss of substance in a lesion with a minimum size of 1 em • Large expansive osteolytic lesion: Renal

carcinoma. thyroid carcinoma. Predilection for pedicle and vertebral body. ~ CTfindings Bone destruction and/or irregularly demarcated bony sclerosis • Soft tissue component.

Variable enhancement after contrast administration.

~ MRI findings Main imaging plane: Sagittal. Bone marrow reaction. Soft tissue component.

Intervertebral disks are usually not affected. T1 hypointensity (natural contrast to mature bone marrow) • STIRhyperintensity (may be absent with calcification) • TI with contrast: Significant enhancement. Whole-body MRJ is useful for staging and searching for the primary tumor. ~ Nuclear medicine Staging. PET: high specificity.

216

Bone Metastases Fig. 5.27 Conventional A-P radiograph of the lumbar spine. Multiple osteoblastic metastases of a breast carcinoma.

Fig.5.28 CTof vertebra L1 (axial). Mixed metastasis of a prostate carcinoma.

217

Bone Metastases fig.5.29 Conventional lateral radiograph of the lumbar spine. Osteolytic

metastasis of a hypernephroma in the posterior vertebra.

fig.5.30 MR image of the lumbar spine (sagittal. STIR).Metastasis with a significant soft tissue component

in vertebra

L3. spreading into the adjacent vertebral body. Colon carcinoma.

218

Bone Metastases Fig. 5.31

MR image of the lumbar spine (sagittal. T2). Metastasis of a bronchial carcinoma in the posterior vertebral body of L5.

Fig.5.32 MR image of the thoracolumbar junction (sagittal. T1) in the same patient as in Fig. 5.3.

219

Bone Metastases

b

....- .... .;

'.. ... t

.

.et .. f ~

'~"

.'. _ .•t· t ~.

~:tl". ) .;. , J'II.

'.'

•

Rg. 5.330, b MRimage ofthe thoracolumbar junction (sagittal, T1 with contrast [al. diffusion-weighted [b)). showing posterior enhancement in vertebra T12. Anterior necrosis is present. Diffusionis not restricted (b). so this is an osteoporotic vertebral collapse. Clinical Aspects ............................................................................................ ~ Typical presentation Pain (especially with exercise and improving significantly with rest. invariably increasing pain consistent with an incipient insufficiency fracture) • Angular deformity. Pathologic vertebral collapse' Radiculopathy. myelopathy (extradural spinal cord compression) • Occurs in order of decreasing frequency in the thoracic (70%), lumbar (20%), and cervical spine. ~ Therapeutic options These depend on the primary tumor. Radiation therapy' Chemotherapy. Surgical management (with neurologic symptoms) • Vertebroplasty • Immunotherapy (experimental).

220

Bone Metastases Differential Diagnosis

............................................................................................ Acute vertebral collapse

in osteoporosis

- Cannot be clearly distinguished from pathologic vertebral collapse (bone marrow edema) - Follow-up examination: Edema will remain unchanged in a pathologic fracture but will regress in an osteoporotic fracture - DWI: Reduced diffusion indicates benign lesion; increased diffusion indicates malignancy - Fluid sign

Primary bane tumors (rare, monostotic)

Hematopoietic tumors (lymphoma, plasmacytoma) Circumscribed bane marrow inhomogeneity

- Fat fibrosis in older patients, red bone marrow indicates increased hematopoiesis - Signs of a benign lesion include: Intact posterior wall and/or sparing of the posterior vertebral elements,

no soft tissue component Selected

References

Dominkus M. Surgical therapy of spinal melastases. Orlhopade. 1998: 27: 282-286 Herneth AM et .11.Diffusion weighted imaging for bone marrow pathologies. Em J Radial 2005: 55: 74-83 Link TM: Spinal metastases. Value of diagnostic procedures in the initial diagnosis and

follow-up. Radiologe 1995: 35: 21-27 Lodwick GS. Determining growth rates of focal lesions of bone from radiographs. Radiology 1980: 134: 577-583 Moulopou!os LA. MR prediction of benign and malignam vertebral compression fractures. J Magn Reson Imaging 1996; 6: 667-674 Yoshida S. The generation of anti-tumoral cells using dentritic cells from the peripheral bloood of patients with malignant brain tumors. Cancer Immunollmmunother 2001; 50:321-327

221

Definition

............................................................................................

• Epidemiology Most common primary malignant bone rumor. Occurs in people over 60 years. • Etiology, pathophysiology, pathogenesis Solitary myeloma (plasmacytoma): A single lesion as opposed to multiple myeloma • The vertebral body and posterior elements are the most common sites of plasmacytoma. Plasma cell infiltration of the medulla. Imaging Signs

............................................................................................

• Modality of choice Conventional radiographs.

MRI(Tl and STIR).

••. General

One or more sharply demarcated osteolytic subcortical lesions. • Radiographic findings Findings are normal in early stages or diffuse osteopenia • Solitary (plasmacytoma) or multiple (multiple myeloma) round, smoothly demarcated osteolytic lesions • Endosteal bony destruction. Vertebral body compression. Secondary sclerosis (after vertebral fracture, radiation therapy, chemotherapy). • CTfindings Osteolysis arising in the medulla. Soft tissue tumor. Sclerotic in 3% of cases. Can infiltrate the intervertebral disk (see also Chordoma) • Minimal enhancement.

• MRI findings Tl hypointensity (isointense to muscle) • Moderate enhancement after contrast administration. Soft tissue tumor. T2 hyperintensity (possibly inhomogeneous) • STIRhyperintensity (diffuse or local). •.. Nuclear medicine Bone scan is typically normal (only sclerotic lesions are positive) • FDG-PET: Active multiple myeloma can be precisely identified. Clinical Aspects

............................................................................................

• Typical presentation Asymptomatic (in 20% of cases) • Anemia (multiple myeloma) • Bence Jones proteinuria. Amyloidosis. Local pain. Vertebral collapse. Electrophoresis (monoclonal gammopathy). • Therapeutic options Radiation therapy (plasmacytoma) • Chemotherapy (multiple myeloma) • Bisphosphonate therapy. Bone marrow transplantation (multiple myeloma). • Course and prognosis Plasmacytoma: Average survival is 10years. Multiple myeloma: Average survival is 3-4 years.

222

Multiple Myeloma flg.5.34 General fatigue and exhaus· tion. with markedly raised erythrocyte sedimentation rate. Conventional lateral radiograph. Multiple osteolytic lesions in vertebrae Ll-LJ and LS.

MR image of the thoracic spine (sagittal. T1 with contrast). The bone marrow is diffusely permeated with hy· perintense enhancing lesions. Vertebral collapse at several sites in the middle thoracic spine.

Fig.5.35

223

Multiple Myeloma Fig.5.36 MR image of the thoracic and lumbar spine (sagittal. T2 with fat suppression). Nodular lesions are present throughout the bone marrow. Normal bone has largely been replaced in the middle thoracic spine.

Fig.5.37 Pelvic a (axial). A circumscribed lytle tumor is present in the left lateral mass. There is no soft tissue tumor.

224

Multiple Myeloma

C'

Differential Diagnosis Metastasis

3

- Disk not infiltrated

(usually)

o

~

Aggressive hemangioma Vertebral collapse in osteoporosis

- Follow-up - OWl

examination

Selected References Baur A. The diagnosis of plasmocytoma with MRT. Radiologe 2000; 40: 716-722 Rand T. Percutaneous radiologically-guided vertebroplasty in the treatment of osteoporotic and tumorous spinal body lesions. Radiologe 2003; 43: 723-728 Sirohi B. Multiple myeloma. Lancet 2004; 363: 875-887

225

Definition ............................................................................................ •

Epidemiology

Rare malignant tumor derived from the notochord. Peakage40-60years. Twice as common in men than in women. Occurs in order of decreasing frequency in the sacral region (50%), sphenooccipital region (30%),and cervical spine. •

Etiology, pathophysiology,

pathogenesis

Chordomas arise from remnants of the notochord (third to seventh week of embryonal development) which arises anterior to the neural tube (sella to coccyx) • The tumor destroys the vertebral body (causing vertebral collapse and secondary sclerosis) • Locally aggressive and metastasizes early • Metastases occur in about 50% of cases (lung, liver, bone, lymph nodes) • Can spread into the intervertebral disk. Calcifications (approximately 40-60% of cases) along the midline, mucoid material. Three histologic types: Conventional, chondroid, dedifferentiated. Imaging Signs ............................................................................................ •

Modality of choice

Conventional radiographs. Cf (spread in bone) • MRI(spread in soft tissue, involvement of neurovascular structures). • General

Bony destruction. Infiltration of the nerve roots and adjacent soft tissue structures • Calcification, fibrosis, cystic necrosis. •

Radiographic

findings

Circumscribed bony destruction (aggressive) • Calcification. line, from sacrum to sphenooccipital • Cffindings

Typical site: Mid-

region.

Hypodense, osteolytic tumor with matrix calcifications (40-60% of all cases) •

•

Slight to moderate enhancement after contrast administration. partment • Sclerosis at tumor edges. MRI findings

Soft tissue com-

Inhomogeneously structured multilobulated osteolytic tumor. Tl hypointensity or hyperintensity; T2 hyperintensity (hyperintense to disk) • Calcifications (Tl and T2 hypointensity) • Slight to moderate enhancement. Clinical Aspects ............................................................................................ ~ Typical presentation Pain. Paresthesias (nerve root infiltration) • Vertebral collapse (pain, angular deformity) • Chromosome abnormalities. • Therapeutic

options

Resection. • Course and prognosis High rate of recurrence (90%) • 5-year survival rate is 80% • lO-year survival rate is 40%. 226

Chordomo Flg.5.38 Patient with six-month history of increasing pain in the sacral region. Conventional

A-P radiograph

of the

sacrum. Geographic lytic lesion.

Fig.5.39 Pelvic CT (axial). Sharply demarcated lobulated sacral lesion with large anterior extra osseous soft tissue tumor.

227

Chordoma

Pelvic MR image (sagittal. T2). large in homogeneously structured solid tumor arising from the sacrum and spreading anteriorly. Impression of the bladder. Lesion has a pseudocapsule. Fig.5.4O

Differential Diagnosis ............................................................................................ Metastases

- Later age - Multifocal

Giant cell tumar

- T2 hypointensity - Hemorrhages may be present

Chondrosarcoma

- Primarily in the posterior spine. cartilage matrix. Chondroid chordoma can be differentiated only on histological examination.

Plasmacytoma. lymphoma. neurogenic tumors Malignant fibrous histiocytoma Selected

- Dedifferentiated chordoma can be differentiated only on histological examination

References

Diel J. The sacrum: pathologic spectrum, multimodality imaging. and subspecialty approach. Radiographies 2001 ; 21: 83-104 Flemming DJ.Primary tumors of the spine. Semin Musculoskelet Radio12000; 4: 299-320 Pease AP. Radiographic, computed tomographic and histopathologic appearance of a presumed spinal chordoma in a dog. Vet Radiol Ultrasound 2002; 43: 338-342 Wacker A. Chordomas-diagnostic steps and therapeutic consequences. Dtsch Med Wochenschr 2002; 127: 1389-1391

228

Definition

............................................................................................ • Epidemiology Rare highly malignant rumor (round-cell sarcoma) occurring in childhood and adolescence. Age 5-20 years. • Etiology, pathophysiology, pathogenesis Closely related to PNET• Permeative osteolytic tumor arising from the medulla, usually with a large soft tissue component. The intervertebral disk is spared. Arises from the vertebral body (occasionally from two). Only 5% of lesions are sclerotic. Extraosseous soft tissue component in over 50%of cases. Metastases (lung, bone, lymph nodes) arise in over 20% of cases. Imaging Signs ............................................................................................

• Modality of choice Conventional radiographs, CT(diagnosis) • MRI(extent of tumor) . ••. General

Aggressive permeative (moth-eaten) osteolysis. Periosteal reaction. Softtissue component (50% of lesions), • Radiographic findings Permeative bony destruction with a broad transitional zone. Periosteal reaction ("onion peel" appearance, "hair on end," Cadman triangle) on the vertebral bodies is often not distinct. Compression franure. • CTfindings Bony destruction. Infiltration of paravertebral structures. Soft tissue component. • MRI findings T1 hypointensity. significant enhancement after contrast administration. T2 and STIRhyperintensity • Evaluation of soft tissue component. Infiltration of paravertebral and intraspinal structures • Caution: Hemorrhage and necrosis can alter the appearance of the lesion . •.. Nuclear medicine Pronounced radionuclide uptake (searching for metastases). Clinical Aspects

............................................................................................ • Typical presentation Pain. Fever and leukocytosis (mimics osteomyelitis) • Swelling. Developmental anomaly. Pathologic fractures present in over 10%of cases. • Therapeutic options Preoperative chemotherapy (goal: 90% reduction in tumor size); combination modality therapy. Resection followed by chemotherapy . •.. Course and prognosis In 50% of cases with localized disease. survival is good. Rate of tumor recurrence is over 15%.

229

Fig. 5.41 Fatigue, slightly elevated temperature. leukocytosis. Conventional lateral radiograph oi the thoracic spine (detail). Moderately sclerotic anteriorly compressed vertebral body. Tumor has penetrated

the posterior cortex. The

matrix is highly inhomogeneous, a sign of osteoblastic and osteolytic posterior bone remodeling.

Fig.5.42 a of the thoracic spine (axial). Large right anterolateral soft tissue tumor with impression of the trachea. Lesion extends to the aortic arch.

Ewing Sarcoma CT of vertebra T8 (axial. bone window). Extensive osteolysis of the vertebral body with paravertebral tumor masses isodense to soft tissue.

Fig.5.43

Differential Diagnosis ............................................................................................ Neuroblostoma cell histiocytosis

Langerhans

- PNET can only be distinguished examination - More geographic

by histologic

lesions

Osteosarcoma

- 80% involve matrix calcification

Eosinophilic granuloma

- Histiocytosis

Osteomyelitis

- Fever. leukocytosis. elevated erythrocyte sedimentation rate - Intervertebral disk also affected

Selected

X

References

Donaldson 55. Ewing sarcoma: radiation dose and target volume. Pediatr Blood Cancer

2004:42:471-476 Flemming OJ.Primary tumors orthe spine. Semin Musculaskelet Radio12000: 4: 299-320 Greenspan A. Remagen W. Differential

Diagnosis of Tumors and Tumor-like

Lesions of

Bones and Joints. Lippincott-Raven 1998 Hoffer FA. Primary skeletal neoplasms: osteosarcoma and ewing sarcoma. Top Magn Reson Imaging 2002; 13: 231-239

231

Definition • Epidemiology Peak age 30-70 years. 85 % are non-Hodgkin lymphomas « 80% are Bceillymphomas) • Initial manifestation is in bone (accounting for 4% of primary bone tumors) • Secondary manifestation (30% of systemic lymphomas metastasize to bone). • Etiology, pathophysiology, pathogenesis Lymphoreticular neoplasm. Secondary involvement (bone to leptomeninges) • Lesions are encountered in order of increasing frequency in bone. at extradural sites, at intradural sites. and in bone marrow. Lesions are highly variable in appearance, rendering differential diagnosis difficult. Imaging Signs

............................................................................................

• Modality of choice Conventional radiographs and cr (bony structures) • MRIwith contrast (leptomeningeal and intramedullary lesions). • General Coution: Because of their highly variable appearance, lymphomas can mimic many other disorders. • Radiographic findings with bony lesions Osteolysis. Rarely sclerosis ("ivory" vertebral body). • cr findings with bony lesions Permeative bony destruction (osteolytic and. less often, sclerotic). Usually multisegmental with infiltration of the disk interspaces • Soft tissue component. • MRI findings with bony lesions T1 hypointensity. T2 hyperintensity • Dynamic contrast MRI shows rapid enhancement. Soft tissue tumor. Homogeneous enhancement after contrast administration.

• Nuclear medicine with bony lesions Bone scan is abnormal, showing increased uptake. FOG-PETis used for staging and follow-up of treatment. • cr findings with leptomeningeal and/or intramedullary lesions Solid tumor mass that may exhibit bony infiltration. Homogeneous enhancement after contrast administration.

• MRI findings with leptomeningeal and/or intramedullary Tumor mass: - On T1: hypointense to isointense. - On T2: isointense to hyperintense (tumor and edema). - On T1 with contrast: pronounced enhancement. Thickened nerve roots.

232

lesions

Lymphomo

Fig.5.44 Conventional A-P radiograph of the thoracic spine. Sclerosis in lymphomatous vertebra T5 ("ivory" vertebral body). Paravertebral soft tissue appears broad· ened.

Fig.5.45 Conventional lateral radiograph of the lumbar spine. Sclerosis in lymphomatous vertebra L1 ("ivory" vertebral body). The sclerosis is highly inhomogeneous. Isolated lytic areas are present.

Clinical Aspects

............................................................................................ • Typical presentation Uncharacteristic

back pain .

•.. Therapeutic options Lymphomas typically respond well to chemotherapy and/or radiation therapy. Surgical decompression is indicated for acute neurologic symptoms.

233

Lymphoma

fig.5.46 CTof the thoracolumbar junction (A-P). Mixed lymphoma.

Fig.5.47 MR image of thoracolumbar junction (coronal STIR).Hyperintense lymphoma in vertebra L3.

234

Lymphoma

.

\.',/, ~

,,, '1,.'.

"

.,.•.1

..

.'

..••

,"It

,

.'

.

Fig.5.48 MR image of T12 (axial, T1 with contrast), The solid areas of the lymphoma show significant enhancement. Osteolytic necrotic areas are also present. A fine mantle of soft tissue tumor surrounds the vertebral body, On the left side, the tumor extends into the vertebral arch.

f .- .• .•.•

,

\

Fig.5.49 MR image of the sacrum (sagittal, T1), Epidural soft tissue mass with cortical destruction.

235

Lymphoma Fig.5.50 Bone scan. Lymphoma appears as a "hot spot" in vertebra L3. Lymphoma is also visualized in the right anterior iliac crest.

Differential Diagnosis ............................................................................................

Bony

- Metastases - Paget disease ("ivory" vertebral - Langerhans cell histiocytosis

Leptomeningeal and/or intramedullary

body)

- Hematoma

- Metastasis - Meningitis - Astrocytoma - Ependymoma

Selected Drevelegas

References A. Imaging

of primary

bone tumors

of the spine. Eur Radiol 2003;

13:

1859-1871 Murphey

MD. From the archives of the AFlP. Primary tumors of the spine: radiologic

pathologic correlation. Radiographies 1996; 16: 1131-1158

236

Definition ............................................................................................ ~ Epidemiology Peak frequency Most common

C' 3 o Vi

is at 30-40 years. These account for 25% of spinal tumors· intradural and extramedullary tumors • Predilection for the

thoracic spine. ~ Etiology, pathophysiology, pathogenesis Occurrence in neurofibromatosis type II: - Tumors arising from the Schwann cells of the nerve sheaths. - Tumors have a capsule. - Usually benign; malignant degeneration is rare. _ Usually small encapsulated tumors. rarely giant Schwannomas (> 2.5 em) with extraspinal components (especially in the lumbosacral and intrasacral regions). Occurrence in neurofibromatosis type I: - Neurofibroma. - Arising directly from the nerve fibers (surrounded by nerve fibers). - No capsule. - Malignant (sarcomatous) degeneration may occur. Histology: - Type A schwannoma (Antoni): Densely packed spindle cells. _ Type B schwan noma (Antoni): Sparse. myxomatous tissue structure, lular. _ Neurofibroma:

hypocel-

Increased connective tissue content. inclusion of nerve roots.

Imoging Signs ............................................................................................ ~ Modality of choice MRI: - Sagittal: T1 with and without contrast. T2. - Axial: TI with contrast. n. - Coronal: Course along the nerve roots. _ Examination should include cerebrum (cranial nerve schwannomas occur in neurofibromatosis type II). Conventional radiographs and CT: _ Preoperative evaluation of bony destruction in giant schwan noma. - Evaluation of spinal stability. ~ Radiographic findings Benign erosion of the posterior margins of the vertebral body ("scalloping") • Widening of the neural foramina. Erosion of the pedicles. ~ CTfindings Hypodense enhancing paraspinal and/or intraspinal mass. Fusiform expansion of the nerve roots. CT myelography. CSF now is obstructed.

237

Nerve Sheath Tumors

Fig. 5.51 Patient with history of increasing radicular deficits for several months with lateral hypesthesia in the thigh. weakness while extending the leg. and early signs of quadriceps atrophy. MR image of the lumbar spine (sagittal. T2). The bony nerve root canal of L5 is widened. but not eroded. It is filled by a structure isointense to the nerve roots lying cranial and caudal to it.

Fig.5.52 MR image of L5 (axial. 12). Image shows left lateral intraspinal extension of the mass.

~ MRI findings General: - Intradural extramedullary mass (rarely intramedullary). - Dumbbell-shaped extension of large tumors across the neural foramina into the extraspinal region. - Extraspinal components are cystic. - Schwannoma: Sharply demarcated. encapsulated. eccentric. - Neurofibroma: Encasement and/or fusiform expansion of the posterior nerve root. Tl: - Signal is isointense to slightly hyperintense to the spinal cord and slightly hyperintense to (SF. - Usually significant enhancement after contrast administration. occasionally homogeneous. occasionally heterogeneous ring enhancement.

238

Nerve Sheath Tumors T2: - Schwannoma: Usually a hyperintense mass. - Neurofibroma: Heterogeneous signal behavior due to cysts. hemorrhage. or collagen deposits. - Signs of malignant (sarcomatous) degeneration (very rare): Increase in tumor size • Tumor size exceeding 5 cm • III-defined margin with infiltrative growth. Heterogeneous signal behavior.

Clinical Aspects ............................................................................................ • Typical presentation Radicular pain. Motor weakness. Unsteady gait. Sensory deficits. Bladder and bowel dysfunction . • Therapeutic options Surgical tumor resection (not indicated in asymptomatic patients with neurofibromatosis type I) • Small nerve sheath tumors are easily resected. Neurofibromas lack a capsule and extend into the extraspinal region. often rendering total resection unfeasible. Resection can result in an iatrogenic neurologic deficit as

functioning nerve fibers are usually resected along with the tumor.

Subtotal re-

section carries a risk of recurrence.

Differential Diagnosis ............................................................................................ Disk prolapse.

sequestration

- No widening of the neural foramina - Associated with degenerative changes in the vertebral bodies - Does not enhance

Meningioma

- Broad base in contact with the dura with "dural tail" sign (adjacent dura mater enhances after contrast

administration) - Usually isaintense to the spinal cord on T2-weighted sequences

Filum cenninale ependymoma

- Different peak age (40-60 years) - Both may occur in neurofibromatosis type 11;morphologically they are practically indistinguishable

Selected References Conti Pet al. Spinal neurinoma: retrospective analysis and long-term outcome or 179 consecutively operated cases and review or the literature. Surg Neurol 2004; 61: 34-43 Khong Pet .11. MR imaging or spinal tumors in children with neurofibromatosis

I. AJR AmJ

Neurorad 2003: 180:413-.417 Sridhar K et .11. Giant invasive spinal schwannoma:

definition

and surgical management.

J Neurosurg 2001: 94: 210-215

239

Definition ~ Leptomeningeal metastases Drop metastases from intracraniol tumors: In children. these occur primarily in medulloblastoma and PNETs• In adults. primarily in glioblastoma. Metastases of systemic extracranial tumors occur primarily in breast and bronchial carcinoma, lymphoma. and melanoma. Benign tumors can also produce leptomeningeal metastases (in children) • Predilection for the lumbosacral region. ~ Intramedullary metastases Rare. Most common in bronchial carcinoma. followed by breast carcinoma. melanoma. and lymphoma; rarely in colon and renal cell carcinoma. Predilection for the thoracic spine. Imaging Signs

............................................................................................

~ Modality of choice MRI: - Sagittal: Tl with and without contrast. T2. STIR. - Axial: Tl with and without contrast. T2. Conventional radiographs and Cf: - Demonstrates associated vertebral metastases. CSFexamination: - Detects malignant cells in leptomeningeal metastasis. ~ Radiographic findings Demonstrates associated bony metastases (lytic and sclerotic lesions). ~ Cffindings Used for diagnosing associated bony metastases. Where MRIis contraindicated. Cf myelography can demonstrate nodular tumor metastases in leptomeningeal metastatic disease. ~ MRI findings Leptomeningeal metastases: - Nodular swellings in the meninges. - Agglutinated thickened cauda equina and/or nerve roots. - The nodules enhance and images also show diffuse leptomeningeal enhancement resembling icing on a cake. Intramedullary metastases: - Usually small tumors limited to a single segment. - Often located anterolaterally. - Circumscribed expansion of the spinal cord. Hypointense on T1. hyperintense on T2: - Hemorrhage produces an inhomogeneous signal. - Marked homogeneous enhancement.

- Small lesion with disproportionately large amount of associated edema. - Metastases to the vertebral bodies. - Homogeneously decreased signal on Tl-weighted images.

240

Leptomeningeal

History of surgery for a melanoma in the back a few years ago. The patient complained of increasing conus medullaris and cauda equina symptoms with pain within the last few months. MR image of thoracolumbar region (sagittal. T2) shows nodular deposits on the fibers fig.5.53

and Intramedullary

Metastases

MR image of the thoracolumbar spine (sagittal, T1). Mixed pattern of diffuse and indistinct nodular enhancement along the thickened fibers of the cauda equina. Findings suggest leptomeningeal metastases. fig.5.54

of the cauda equina.

- Increased or decreased signal on T2-weighted - Soft tissue component with disrupted cortex.

images.

Clinical Aspects

............................................................................................ ~ Typical presentation Leptomeningeal metastases: - Asymptomatic for a long time. - Headache. - Radicular pain. - Distal lesions produce cauda equina syndrome.

241

Leptomeningeol

ond Intramedullory

Metostoses

Flg.5.55 Increasing spasticity in the presence of known breast carcinoma. MR

image (sagittal. STIR)shows a hyperintense lesion at the level of C2-C3 with marked edema and a second suspicious

lesion at the level of the C6-(7 disk interspace.

Intramedullary metastases: - Dissociated sensory deficits. - Flaccid or spastic paresis . • Therapeutic options Leptomeningeal metastases: - Radiation therapy where CSFflow is obstructed. - Intrathecal chemotherapy. Intramedullary metastases: - Steroids. - Radiosensitive tumors are treated with radiation therapy. - Chemotherapy. - Vertebrectomy . • Course and prognosis Prognosis is poor: mean survival time without therapy is 3-6 weeks.

242

Leptomeningeal and Intramedullary Metastases Differential Diagnosis Leptomeningeal metastases

- Arachnoiditis - Usually the meninges and fibers of the cauda equina show homogeneous linear enhancement. rarely nodular enhancement - History (surgery, trauma, or infection) - Sarcoidosis, Wegener granulomatosis - Enhancing leptomeningeal lesion usually accompanied by enhancing intramedullary focal lesions (see chest radiograph)

Intramedullary metastases

- Primary intramedullary tumors such as astrocytoma and ependymoma - History (is there a known primary extraspinal tumor?) - Often extends across several vertebral segments

Spinal infarction

- Acute onset of symptoms - Follow-up MRI arrer 2-3 weeks shows regression of the mass effect and enhancement after contrast administration

Multiple sclerosis

- Follow-up MRI after approximately 4-6 weeks shows complete regression of enhancement in the lesions and no increase in size

Transverse myelitis

- Follow-up MRI after 6 weeks shows decreased spinal cord swelling and intramedullary signal alteration

Selected References Gamori JM et .11.leptomeningeal metastases: evaluation by gadolinium enhanced spinal magnetic resonance imaging.J Neuroonco11998: 36: 55-60 Loughrey GJ et .11.Magnetic resonance imaging in the management of suspected spin
Schiff 0 et al.lnrramedullary spinal cord metastases: come. Neurology 1996; 47; 906-912

Clinical features and treatment out-

243

Definition ~ Epidemiology Peak incidence is at 40-60 years. Second most common intradural extramedullary tumor (after nerve sheath tumors) • Increased incidence with neurofibromatosis

type II, occurs in younger

patients

• More common

in women

than

men(4:1 t08:1). ~ Etiology, pathophysiology, pathogenesis Benign slow-growing tumor derived from arachnoid cells. Rarely exhibits intradural and extradural or solely extradural growth (5% of lesions) • Predilection for the thoracic and cervical spine. Imoging Signs ~ Modality of choice MRI:

- Sagittal: Tl with and without contrast, n. - Axial: Tl with contrast, n. Conventional radiographs and CT: - Helpful in evaluating bony destruction with larger tumors. ~ Radiographic findings Benign erosion of the posterior margins of the vertebral body ('·scalloping·') • Widening of the neural foramina. Erosion of the pedicles. ~ CTfindings Solid. smoothly demarcated mass isodense to muscle. Calcifications often occur with the psammomatous subtype. CTmyelography is useful where MRIis contraindicated.

~ MRI findings Usually a nodular intraspinal mass develops, plaquelike growth is rare. Tumor compresses and displaces the spinal cord. Broad area of dural contact. Extradural tumors show a hypointense band between tumor and spinal cord. Where both intradural and extradural components are present, the tumor may grow in an hourglass configuration. Tl:

- Isointense to slightly hyperintense. - Enhancement after contrast administration is variable and inhomogeneous

where calcifications are present. - Adjacent dura enhances with contrast in 5% of cases ("dural tail" sign).

n: - Isointense to hyperintense. - Calcified rumors are hypointense.

244

Meningioma Flg.5.56 A 67-year·old woman with history of pain for several months. MR image of the thoracic spine (sagittal, T2). Round, hypointense. intradural extramedullary mass.

Fig,5.57 MR image of the thoracic spine (coronal, T1). Intradural extramedullary mass on the left side impressing and displacing the spinal cord.

245

Meningiomo fig.5.58 MR image of the thoracic spine (sagittal. T1 with contrast). Mass shows moderate enhancement.

Fig.5.59 MR image of T11 (axial. T1 with contrast). The mass enhances significantly compared with the spinal cord.

246

Meningioma Clinical Aspects ............................................................................................ • Typical presentation Back pain. Motor weakness. bowel dysfunction .

Unsteady gait.

Sensory deficits.

Bladder and

... Therapeutic options Surgical tumor resection. Tumor may recur following subtotal resection. Supplementary radiation therapy is indicated where total resection is not feasible or with early recurrence of tumor.

Differential Diagnosis ............................................................................................ Disk herniation. sequestration

- Associated with degenerative changes in the vertebral bodies - Na widening of the neural foramina

- Does not enhance Nerve sheath rumors

(schwannoma. neurofibroma)

- Tumor adjacent to or within nerve fibers - Usually hyperintense (schwannoma) on T2-weighted sequences or heterogeneous (neurofibroma) - Cystic components - Different peak age (30-40 years)

Metastases Selected References Gezen F et al. Review of 36 cases of spinal cord meningioma. Spine 2000: 25: 727-731 Kleekamp Jet al. Surgical results of spinal meningioma. Acta Neurochir (Suppl) 1996; 65: 77-8\ Takemoto K et al. MR imaging of intraspinal tumors-capability in histological differentiation and compartmentalization of extramedullary tumors. Neuroradiology 1988: 30: 303-309

247

Definition • Epidemiology Peak age 30-40 years. Most common tumor of the spinal cord and filum terminale in adults (accounting for approximately 40% of intramedullary tumors) • More common in men than women (3:2). • Etiology, pathophysiology, pathogenesis Arises from ependymal cells of the central canal and terminal ventricle. Associated with neurofibromatosis type II. Subtypes: - Inrramedullary: Predilection for the cervical spine, less often thoracic spine. - Extramedullary: Occurs in the filum terminale and conus medullaris (usually myxopapillary subtype). - Metastatic: Spinal metastasis of intracranial primary tumor. Imaging Signs • Modality of choice MRI:

- Sagittal: n, T2, blood sensitive sequence. - Contrast administration: n axial and sagittal. Conventional radiographs and CT: - Helpful in evaluating bony destruction with larger tumors. • Radiographic findings Erosion of the vertebral pedicles • Thinning of the posterior margin of the vertebrae. Scoliosis. • CTfindings Visualization of associated bony changes. CT myelography (only where MRI is contraindicated): Expansion of the spinal cord, obstruction ofCSF flow. • MRIfindings Lesion located in the central spinal cord and exhibiting expansive centrifugal growth. Lesions occurring in the filum terminale show thickened cauda equina fibers and nodular structures but no cysts.

Average longitudinal

extent is across

three to four vertebrae. Often (50% of cases) a large cyst with a small solid component is present. Often associated with syringomyelia. Expansion of the spinal cord.

n: - Usually a hypointense to isointense mass, may also be hyperintense secondary to hemorrhage. - Solid tumor components usually show significant homogeneous, irregularly patchy, or nodular enhancement on the cyst wall. - Hypointense cysts.

T2: - Hyperintense mass aligned parallel to the longitudinal axis of the spinal cord. - There may be a hypointense halo due to hemosiderin deposits ("cap sign"). - Hyperintense cysts. 248

Ependymomo Fig.5.60 A 40-year-old man with paresthesias in both lower extremities and an unsteady gait. MR image of the thoracic spine (sagittal, T2). Round intramedullary mass with marginal hemosiderin deposits. cysts. and associated syringomyelia.

Fig. 5.61 MR image of the thoracic spine (sagittal, 11 with contrast). The tumor shows significant enhancement after contrast administration. The hypointense hemosiderin deposits remain unchanged.

249

Ependymoma Fig.5.62 The patient had had increasing. electric-shocklike pain in the lower back and both legs for several months. This was accompanied by difficulty in emptying the bladder. perianai sensory deficits. and weakness in the legs. MR image of the lumbosacral spine (sagittal. T2) shows an irregular pattern of the cauda equina fibers and a large oval mass at the level of L5-S1.

Fig.5.63 MR image of the lumbosacral spine (sagittal, T1 with contrast). inhomogeneous at the level of L4-LS. The mass at l5-S1 is hypointense, consistent with a cyst.

250

Clinical Aspects ............................................................................................ • Typical presentation Progressive neck and back pain. Paresthesias • Motor weakness. Bladder and bowel dysfunction. Acute paraplegia: With regressive ependymomas of the filum terminale. bleeding can produce a hematoma with mass effect and subarachnoid hemorrhage. • Therapeutic options Laminectomy

and radical

tumor

resection.

Postoperative

radiation

therapy

is

indicated where only subtotal resection is feasible . •.. Course and prognosis Five-year survival rate is between 68% and 95% • Tumor may recur (5-10% of cases), especially following subtotal resection. Follow-up examinations with MRI.

Differential Diagnosis · Astrocyroma

. - Most common

intramedullary

tumor

in children

- Rarely in the filum terminale - Eccentric growth with asymmetrical expansion of the spinal cord - Hemorrhaging

is less common

- Infiltrating - Inhomogeneous

Hemangioblastoma

enhancement

after contrast

admin-

istration - Irregularly patchy, hypointense area due to flow voids - Well-demarcated. significant perifocal edema often present

- Often associated with syringomyelia Metastasis

- Known

Schwannoma (DD: Filum tenninale ependymoma) Lepromeningeal metastases (DD: Filum tenninale ependymoma)

underlying

malignant

disease

- Higher peak age - Widening of the neural foramina - Arises from the root of the cauda equina (extramedullary intradural location) - History (possibly known primary tumor)

Selected References Fine MJ et al. Spinal cord ependymomas: MR imaging features. Radiology 1995; 197: 655-658 Miyazawa

N et al. MRI at 1,5 T of intramedullary

ependymoma

and classification

trast enhancement. Neurorad 2000; 42: 828-832 Schwartz TH et al. Intramedullary ependymomas: clinical presentation. ment strategies and prognosis.J Neurooncol2000;

of con-

surgical treat-

47: 211-218

251

Definition ............................................................................................ ~ Epidemiology Peak age 20-40 years. More common in men than women (3:2) • Most common intramedullary tumor in children (up to 90% of cases). ~ Etiology, pathophysiology, pathogenesis Holomedullary astrocytoma: Lesion extending over the entire length of the spinal cord (rare). Histologic classification: - Pilocytic astrocytoma (more favorable prognosis). - Diffuse fibrillar astrocytoma. Associated with neurofibromatosis type 1 • Predilection for the cervical and thoracic spinal cord. Imoging Signs ............................................................................................ ~ Modality of choice MRI: - Sagittal: n with and without contrast, T2. - Axial: n, n with contrast. - Gradient echo sequence. Conventional radiographs: Scoliosis. Widening of the spinal canal. Erosion of the pedicles, thinning of the posterior margins of the vertebral bodies CT: Visualization of associated bony changes • CT myelography (only where MRI is contraindicated): Expansion of the spinal cord, obstructed CSFflow. ~ MRI findings General: - Expansion of the spinal cord, usually over several segments. - Ill-defined border. - Difficult to distinguish tumor from tumor edema.

n: - Isointense to weakly hypointense mass. - Inhomogeneous enhancement is more obvious in pilocytic astrocytomas than in fibrillar astrocytomas.

n: - Hyperintense intramedullary mass. - Signal inhomogeneities resulting from bleeding, necrosis, or cysts.

151

Astrocytoma flg.5.64 History 01 increasing gait disturbance over several years. MR image of the thoracic spine (sagittal, T2). The spinal cord is expanded in the middie and lower thoracic regions and appears inhomogeneous and faintly hyperintense. The subarachnoid gioma

space is obliterated.

is present

in vertebra

A hemanT3.

fig.5.65 MR image olllO (axial. STIR). Abnormal signals within the spinal cord.

253

Astrocytomo

c:t 3

MRimage of the thoracic spine (Tl with contrast). Slight diffuse

~

enhancement

Fig.5.66

within the spinal cord.

Clinical Aspects ............................................................................................ • Typical presentation Symptoms progress slowly over a period of months to years.

Back pain. Motor

deficits.

Progressive scoliosis. Cervical lesions produce torticollis. Hydrocephalus • Brown-Sequord syndrome: Asymmetric tumor growth produces spastic hemiparesis on one side while reducing pain and temperature sensitivity on

the contralaterai side. Bladder and bowel dysfunction . • Therapeutic options Where tumor progression is very slow with minimal neurologic dysfunction. especially in the infiltrative subtype. one should carefully consider where surgical intervention is indicated. Laminectomy or osteoplastic laminotomy (preferred in children) • Tumor resection and postoperative radiation therapy. Chemotherapy is indicated with subtotal tumor resection and recurrent tumor . •.. Course and prognosis

Five-year survival rate is 58%.

254

Differential Diagnosis ............................................................................................ Ependymoma

- Occurs in rhe center of the spinal cord - More clearly demarcated _ Hemosiderin deposits create a hypointense halo on T2-weighted sequences

Metastases

- History (is there a known primary extraspinal tumor?) - Extent of lesion usually limited to one segment

Gangliaglioma Multiple sclerosis

- In children younger than 3 years

Transverse myelitis

- Follow-up MRI after 6 weeks shows decreased spinal cord swelling and intramedullary signal alteration

Spinal infarclion

- Acute onset of symptoms - Follow-up MRI after 2-3 weeks shows regression of the mass effect and enhancement after contrast administration

C' 3 o 01

_ Follow-up MRI after approximately 4-6 weeks shows complete regression of enhancement in the lesions and no increase in size

Selected References Houten JK. Howard LW. Pediatric intramedullary spinal cord tumors: special considerations. J Neuraoncol 2000: 4?: 225-230 HoutenJK. Cooper PRoSpinal cord astrocytoma: presentation, management and outcome. J Neurooncol 2000: 47: 219-224 Lowe GM. Magnetic resonance imaging of intramedullary spinal cord tumors. J Neuroonco12000: 47: 195-210

255

Definition ~ Epidemiology Usually manifests itself before 30 years (often at 20-30 years) in the setting of van Hippel-lindau

disease.

More common in men than women by a ratio of

2:1 • Accounts for 3-5% of all tumors of the spinal cord. with a predilection for the posterior cervical and thoracic cord.

~ Etiology, pathophysiology, pathogenesis Histologically benign vascular tumor. Seventy to eight percent are idiopathic solitary lesions; 16-25% occur as multiple lesions in von Hippel-Lindau diseased (with retinal and cerebellar hemangioblastomas and abdominal cysts). Associated syringomyelia occurs in 50-70% of cases. Imaging Signs ~ Modality of choice MRI:

- Sagittal: n with and without contrast. n. - Axial: T2. TI with contrast. ~ Digital subtraction angiography (DSA) - Preoperative planning. ~ CTfindings Enhancing nodules, often adjacent intramedullary cysts. ~ MRI findings General: - Small nodule. large cyst. - Superficial site in the spinal cord. usually on the posterior aspect. - Often diffuse spinal cord swelling because of associated edema. - Tumor itself is well demarcated. - Larger tumors contain punctate hypointensities on all sequences. These are

now voids produced by rapidly nowing blood. - Hemorrhages are common. - Associated syringomyelia.

n: - Isointense to hypointense lesion. - Pronounced enhancement.

- Hypointense to hyperintense cyst, depending on protein content.

n: - Hyperintense

nodular mass.

- Associated edema is seen and associated cysts are well demarcated as hyperintensities.

~ DSAfindings - Hypervascular. sharply demarcated tumor. - Visualization of vessels supplying and draining the tumor.

256

Fig.5.67 Patient with known von Hippel-Lindau disease and increasing spastic tetra paresis. MR image of the cervical spine (sagittal. T2). The spinal cord appears swollen and hyperintense (associat· ed edema) from the craniocervical junc· tion to (7- Tl. At the level of C3 there is a hyperintense lesion with a hypo intense halo. There is also a hyperintense mass in the cerebellar vermis. A small hypo intense area (flow void) is seen in the center of this mass.

Fig.5.68 MR image of the cervical spine (sagittal. Tl with contrast). The intraaxial lesions enhance. as do the meninges.

Clinical Aspects ............................................................................................ • Typical presentation Course is insidious; symptoms are exacerbated by associated edema, cysts, andl or syringomyelia. Pain. Scoliosis. Sensory deficits. Paraparesis or tetra paresis • Bowel and bladder dysfunction .

•.. Therapeutic options Complete removal of the tumor resection. Preoperative zation of the vascular feeders may be considered.

superselective

emboli-

257

Hemangiablastoma Fig.5.69 MR image of (4 (axial, Tl with contrast). Enhancing lesions and hypointense signal alterations within the spinal cord. The subarachnoid space is obliterated.

Differential Dlagnasls Astrocytoma

- Isointense or slightly hypointense to spinal cord on noncontrasted Tl-weighted images - No now voids - Enhancement is weak or even absent - Hardly ever cystic - Hemorrhages extremely rare - Poorly demarcated

Ependymoma

- Predilection for craniocelVical junction and lumbar theca - No now voids

Selected

References

Baker KBet al. MR imaging of spinal hemangioblastoma. Lowe GM. Magnetic

AmJ Roenlg 2000: 174: 377-382

resonance imaging of intramedullary

spinal cord tumors.

J

Neuro-

oncol 2000: 47: 195-210 Miller OJet al. Hemangioblastomas and other uncommon intramedullary tumors. J NeurooncoI2000:47: 253-270

258

Definition ............................................................................................ • Epidemiology Rare, potentially life-threatening. common

in men than women.

Caution: Distal neurologic deficits.

Peak age for spontaneous

occurrence

More

is between

40 and 50 years, • Etiology, pathophysiology, pathogenesis Bleeding from the epidural venous plexus. Occurs spontaneously in coagulation disorders and in patients on anticoagulanttherapy • Idiopathic (45% of cases) • Posttraumatic. Imaging Signs

............................................................................................ • Modality of choice Emergency indication for MRI: - Sagittal: Tl, TI. - Axial: TI. - Gradient echo sequence. • CTfindings Hyperdense extradural lesion compressing the dural sac (usually posteriorly). • MRI findings Intraspinal. extradural mass that does not enhance. Sagittal: Biconvex "teardrop" shape. Increased enhancement of the adjacent meninges (differentiation Froman abscess is difficult) • Secondary compressive myelopathy may be seen. Posterior epidural hematoma -

More common.

- Cannot be differentiated From subdural hematoma. Anterior epidural hematoma: - "Curtain sign"-hemorrhage is divided into two parts by the membrane of Trolard (not present in a subdural hematoma). Tl (according to the age oFthe hemorrhage): - Acute: isointense.

- Subacute (after 3-4 days): hypointense in the center, hyperintense on the periphery. - Chronic: markedly hypointense halo of hemosiderin. TI (according to the age of the hemorrhage): - Acute: hyperintense to hypointense. - Subacute (> 5 days till several weeks): hyperintense. - Chronic: markedly hypointense halo. - Gradient echo sequence: better demarcation of the hematoma.

259

Epidural Hematoma

i§=

'"

""is" ...,

o 0;' o

a. •• i:!

Fig. 6.1

Patient with posttraumatic paraplegia in the legs and sensory deficits distal to the level of vertebra T4. CT of T7 (axial). Left lateral posterior hyperdense oval mass compressing and displacing the

dural sac. Flg.6.3 MR image ofT7 (axial. T1). Central epidural hyperintense lesionmethemoglobin.

260

fig.6.2 MR image of the thoracic spine (sagittal. T2). Several elongated epidural lesions with contents of varying intensity lying adjacent to the notably hypo intense dura. Comminuted fracture of T9 with intraspinal fragments and compression of the spinal cord.

Epidural Hematoma

Clinical Aspects

............................................................................................ • Typical presentation Symptoms are identical to those of acute disk prolapse. Severe. often radicular radiating pain at the level of the hemorrhage. Distal neurologic deficits occur within a few hours . • Therapeutic options Rapid laminectomy and removal of the hematoma. Delayed decompression will result in neurologic deficits.

Differential Diagnosis

Metastases

- Concave; anterior lesions that cross the midline are not divided by a membrane - Thickened meninges; associated diskitis or osteomyelitis may be present - Associated pathology in the adjacent vertebral body

Lymphoma

- Homogeneous enhancement

Spina/lipomatosis

- Homogeneous signal intensity. hyperintense on T1

Subdural hematoma Abscess

and T2 Selected References DOfsayet al. MR imagingof epidural hematoma in the lumbar spine. Skeletal Radio12002;

31:677-685 Gundry CR et al. Epidural Hematoma of the lumbar Spine: 18 Surgically confirmed cases.

Radiology1993: 187:427-431 Sklar EMet al. MRIof acute spinal epidural hematomas.J Comput AssistTomogr 1999; 23; 238-243

261

Definition ............................................................................................ ~ Epidemiology Intradural arteriovenous malformation (AVM): Usually manifests before 30 years of age. Spinal dural AV fistula: Usually manifests after 40 years of age. ~ Etiology, pathophysiology, pathogenesis Abnormal direct communication between an artery and a vein, without a capillary bed between them. Classification: - Congenital AVM: Glomerular (intramedullary nidus). plexiform. or juvenile (complex AVMextending across several vertebral segments). fistulous, (extramedullary intradural) • "High-flow" vascular malformation. - Acquired AVM (> 60% of cases): Spinal dural AVfistula. "Low-flow" vascular malformation. Spontaneous, posttraumatic, postinflammatory, or postoperative • More than half of all lesions occur in the thoracolumbar spine.

Imoging Signs ............................................................................................ ~ Modality of choice MRI:

- Sagittal: T1 with and without contrast, 12. - Axial: 12. - MR angiography after contrast administration. DSA. ~ MRI findings Expanded blood vessels in the spinal canal (intramedullary, intradural, dural), hypointense on T1 and 12 (flow void), hyperintense after contrast administration • Blood breakdown products post hemorrhage and/or rupture. A fistula may be seen. Spinal cord is expanded due to congestive edema (hyperintense on 12-weighted images) • Spinal cord atrophy due to ischemia. bleeding. or chronic compression.

~ MR angiography findings Visualization of vascular structures supplying and draining the malformation. ~ CTmyelography findings Visualization of dilated intradural vessels. ~ DSAfindings Detailed preoperative evaluation of vascular structures • Differentiation

"high-flow" AVMsfrom "low-flow" AVMs• Visualization of fistulas.

262

of

Arteriovenous Malformation Fig.6.4 Child with permanent torticollis and progressive spastic quadriplegia. MR image of cervicothoracic region (sagittal. T2). Atypical ectatic vascular structure causing posterior impression of the spinal cord at the level of C4 through Tl. Addi· tional abnormal flow voids are seen on the anterior surface of the medulla oblongata.

Fig.6.5 MR image of C4 (axial. T2). Two large vascular cross-sections are present posterior to the compressed spinal cord.

263

Arteriovenous Malformation Flg.6.6 MR myelography (coronal. T12). The vascular malformation is well demarcated against the hyperintense (SF.

Flg.6.7 MR angiography (coronal with contrast). Image shows the relationship of the AVM to the vessels supplying and draining it.

264

Clinical Aspects ............................................................................................ • Typical presentation Intradural AVM - Usually manifests itself after age 30 years. - Subarachnaid hemarrhage: Acute onset of severe headache. meningism. and photophobia. - Intraparenchymal hemarrhage: Sudden pain. acute neurologic dysfunction. - Mass effect: Growth of the AVMcompresses nerve tissue. leading to neurologic deficits. Spinal dural AVfistula: - Usually manifests itself after age 40 years. _ Slowly progressive symptoms over a period of months to years. - Progressive weakness in the legs and bladder and bowel dysfunction. - Pain that increases with motion or change of position. Foix-Alajouanine syndrome (subacute necrotizing myelitis): - Extreme course occurs only in a few patients. - Characterized by rapidly progressive myelopathy due to venous thrombosis (DO: Intermittent claudication. spinal stenosis) . •.. Therapeutic options Endovascular embolization. Open ligation. The two procedures are often used

~ '"c: "Q .., o ..,o

,,' 0..

'"~

in combination.

Differential Diagnosis Intramedullary cavernaus malfarmatian

Hemangiablastama

- Inhomogeneous signal in the center on T1 and 12 images due to slow-flowing blood. Blood breakdown products of varying age. hypointense halo from hemosiderin deposits on 12-weighted images - Significant expansion of the spinal cord. associated cyst or syrinx

Selected References Cullen 5 et .11.Spinal aneriovenous shunts presenting before 2 years of age: analysis of 13

cases. Childs Nerv Syst 2006: 22: 1103-1110 Koch C. Spinal dural arteriovenous

fistula. Curf Opin Neural 2006:

19: 69-75

Meisel HJer .11.Modern management of spinal and spinal cord vascular lesions. Minim In-

vasive Neurosurg 1995: 38: 138-145 Thron A et al. Spinal arteriovenous malformation. Radiologe 2001; 41: 949-954 Tomlinson FH et al. Arteriovenous fistulas of the brain and the spinal cord. J Neurosurg

1994:80: 178-179

265

Cf

'""c: Q ...

o ;;;. o ...

Q.

'" ~

Definition ............................................................................................ • Epidemiology Rare. More common in arteriosclerosis. aortic dissection, thromboembolic disease. vasculitis. autoimmune disease. syphilis. diabetes mellitus. cardiac arrest. caisson disease. vascular compression due to tumor or trauma. prolapsed disk . iatrogenic cases (aortic surgery, contrast agent toxicity). • Etiology, pathophysiology, pathogenesis Ischemia in the area supplied by the anterior spinal artery (receives blood from branches of the aorta, supplies the anterior two-thirds of the spinal cord). Rarely in the area supplied by the posterior spinal arteries. Predilection for the lower thoracic cord and conus medullaris.

Imaging Signs ............................................................................................ • Modality of choice Emergency indication for MRI: - Sagittal (T!, T2) and axial (T2) slices. - DWI, axial and sagittal: Hyperintense signal in the acute stage. CSFexamination: - This can exclude innammatory and/or infectious disorders of the spinal cord. • CTfindings CT myelography is used where MRIis contraindicated; otherwise CT is not suitable. • MRI findings DWI: -

Hyperintense

signal immediately

after ischemia.

very sensitive.

T2:

- Acute; Note that the latency period is longer than in cerebral ischemia. - Sagittal: Linear signal increase in the spinal cord with slight expansion. - Axial: Signal increase in the anterior and posterior spinal cord, primarily in the gray matter (an isolated "owl's eye" sign may be seen in the anterior horn), usually bilaterally in the paramedian region (symmetric or asymmetric). - Chronic: Hyperintense glial scar with circumscribed spinal cord atrophy. - Associated vertebral infarction: Hyperintense signal alteration in the vertebral body at the same level and supplied by the same artery. T!: - Subacute: Enhancement is detectable for several weeks. - The periphery may appear slightly hyperintense where there is hemorrhagic transformation.

MR myelography: - Conventional angiography shows abnormal vascular structures due to an underlying AVM. - Visualization of abnormal vascular structures with the option of embolization.

266

Arterial Spinal Card Infarction

Fig. 6.8

Bilateral paresis in the arms fol-

lowing surgical correction of an aortic aneurysm. MR image of the lower cervical spine (sagittal. anterior

T2). Hyperintensity

spinal cord at

in the

(5-(8.

~ '"c": Q ..,

o i;;' o ..,

0..

'"<:l

Fig.6.9

J

MR image of the lower cervical

spine (sagittal.

diffusion-weighted):

Hyperintensity

in parts of the lesion.

>.

\\ \.

267

Arterial Spinal Cord Infarction ~

::: ~

..,

Fig.6.10 MR myelography of C7 (axial, T2). Hyperintensity mainly in the anterior horns .

o

;;;.

o

~ ~

Flg.6.11 MR angiography (coronal). Atypical tortuous vessel.

268

Arterial Spinal Cord Infarction Clinical Aspects

............................................................................................ • Typical presentation Paraparesis or tetraparesis. either with acute onset or initially flaccid and then

spastic. Usually burning or stabbing pain at the level of the affected segment (80% of all cases) • Anterior inforerion: Dissociated sensory deficit with loss of sensitivity to pain and temperature caudal to the infarcted level. Posterior infarction: Impaired proprioception and sensitivity to vibration • Bladder and bowel dysfunction. Cervical: Horner's syndrome . •.. Therapeutic options Medical therapy with aspirin: elimination of vascular compression where indi-

cated • Neurologic rehabilitation. • Course and prognosis Permanent neurologic deficits are common. Immobilization promotes comOfbidities such as pulmonary embolism and infections.

Differential Diagnosis ·

Foix-Alajouanine syndrome (subacute necrotizing myelitis) Spinal cord necrosis due to a thrombosed AVM Myelitis produdng distal neurologic defidts

Guil/ain-Barre syndrome (postinfeerious polyneuropathy)

. - Selective angiography to visualize abnormal vascular structures

- Selective angiography to visualize abnormal vascular structures - Changes in the cord white malter are more pronounced - Inhomogeneous enhancement - Multiple sclerosis - Plaques occur primarily in the lateral spinal cord - Lacks clinical findings of sphincter dysfunction - Reduced nerve conduction velocity

Vasculitis Selected

References

Faigj et al. Vertebral body infarction as a confirmatory sign of spinal cord ischemic stroke. Report of three cases and review of the literature. Stroke 1998: 29: 239-243

Loher TJ et al. Diffusion-weighted MRI in acute spinal cord ischaemia. Neuroradiology 2003: 8: 557-561 Weidauer Set al. Spinal cord infarction: MR imaging and clinical features in 16 cases. Neu-

roradiology 2002: 44: 851-857

269

Definition

............................................................................................

o Epidemiology This is a common complication of spinal surgery (approximately 41 % of cases) • Most common. specific complications include spinal stenosis (lateral approximately 55%. central approximately 15%). recurrent prolapse (extrusion: approximately 15%). arachnoiditis (approximately 10%). o Etiology, pathophysiology, pathogenesis Excessive scarring leading to stenosis of the spinal canal and/or neural foramina • Prolonged or new pain. functional deficits, instabiliry.

Imaging Signs

............................................................................................

o Modality of choice MRI: - Visualizes the morphologic substrate of the complication. - With and without IV contrast agent. o Radiographic findings Angulation. Instability (stress views) • Progressive degeneration. o Cffindings Multidetector Cf for multiplanar reconstruction in the sagittal and coronal planes. Bony changes and degeneration. Limited sensitivity in detecting complications in neural structures and soft tissue. o MRI findings Axial and sagittal (STIR. n, T2) • IV contrast to differentiate recurrent extrusion (no enhancement) from scarring (significant enhancement) • In rare cases. recurrent extrusion will also enhance due to reactive inflammatory changes. High specificity for spinal stenosis. recurrent prolapse. arachnoiditis, (SF fistula. and epidural fibrosis .

•.. Nuclear medicine (SF fistula.

Clinical Aspects

............................................................................................

o Typical presentation Prolonged and/or increased pain. Limited function. Instability. o Therapeutic options Pain therapy (systemic. local interventional. complementary Physical therapy. Revision surgery. Selected

procedures)

•

References

Kim 55. Revision surgery for failed back surgery syndrome. Spine 1992; 17: 957-960 Markwalder TM. Failed back surgery syndrome. Part I: Analysis of the clinical presentation and results of testing procedures for instability of the lumbar spine in 171 patients. Acta Neurochir(Wien) 1993; 123: 46-51

270

Failed Back Surgery Syndrome FIg. 7.1 MR image of L2 (axial. Tl). Postdisk surgery. There is a left lateral round hypointense mass indenting the dural sac.

Fig.7.2

MR image of L2 (axial. Tl with

contrast). Significant enhancement

of the

hypointense area, representing scar tissue with reactive thickening of the nerve root (same patient as in Fig. 7.1).

271

~

Definition

"..•i3

• Epidemiology Peak age 20-40 years. Twice as common in men than in women. • Etiology, pathophysiology, pathogenesis Spontaneous. secondary to intervention (lumbar puncture, postsurgical). posttraumatic. Lossof intradural CSFvolume and pressure. Marfan syndrome (dural defect) .

'"o

-

..•,,' o 0;;' o ...,

..•

Q.

O!

Imaging Signs • Modality of choice MRI:

- Sagittal. - Axial. ••. General

Thickened dura. Enlarged epidural venous plexus. Extradural accumulation of CSF. • CTfindings Enlarged venous plexus (hypodense tubular epidural structures)' Arachnoid diverticulum.

• MRI findings Enlarged venous plexus (signal void) • Extradural fluid accumulation isointense to CSF. Fistula. MRmyelography (arachnoid diverticulum) • Skull MRl: Signs of cerebral hypotension (thickened. enhancing dura mater; subdural hygromas; caudal displacement of the brainstem) . •.. Nuclear medicine

Cisternography (sensitivity 60%). Clinical Aspects ............................................................................................ •.. Typical presentation Severe occipital headache resistant to therapy. nerve, optic nerve)

• Impaired

consciousness.

Cranial neuropathy (abducens Coma (rare).

• Therapeutic options Spontaneous

remission is common, > 75% of cases.

management of the CSFfistula.

272

Fluid substitution.

Surgical

(SF Fistula MR image of the lumbar spine (sagillal. T1). Postoperative extradural defect isointense to (SF at LS-S 1.

Fig.7.3

MR image of the lumbar spine (sagittal. T2). Hyperintensity at the surgi· Fig. 7.4

cal site (extradural

region). Degenerative

disk disease at l5-S1. Posterior disk her· niation at l4-lS.

273

(SF Fistula

~ ~ ~

fig.7.5 Pain after disk surgery. MR image of L5-51 (axial. T2). Signal alteration isointense to (SF along the surgical site communicating with the dural sac: a (SF

•.•.

fistula.

a

~. 1:1 ;;;.

o

~ <;l

Differential Diagnasis Enlarged venous plexus

- Thrombosis - AVM - Spinal stenosis

Pachymeningitis

- Thickened - Idiopathic

Selected

enhancing meninges or infectious

References

Black P.Cerebrospinal fluid leaks following spinal surgery: use of fat grafts for prevention and repair. Technical note. J Neurosurg Spine 2002; 96; 250-252 Eismont FJ.Treatment of dural tears associated with spinal surgery. J Bone Joint Surg Am 1981; 63; 1132-1136

274

Definition Postoperative scar tissue, which can cause spinal stenosis and/or stenosis of the neural foramina (in approximately 7% of cases) • Physiologic repair mechanism secondary to surgical intervention. The extent of scarring depends on the extent of the surgical intetvention

and the patient's immune and inflammatory

response.

Imaging Signs

............................................................................................ • Modality of choice MRI: - Sagittal. - Axial. Ii>

General

Enhancing structures that infiltrate the perineural fatty tissue (note that these may have a mass effect). • CTfindings Enhancing perineural soft tissue structures.

• MRI findings Perineural soft tissue infiltration. Mass effect is occasionally present (DO: Tumor) • Isointense to soft tissue on T1-weighted images, uncharacteristic findings on T2-weighted images. Enhancement after contrast administration (STIR). Clinical Aspects

............................................................................................ • Typical presentation Paresthesias. Motor deficit (rare) • Radiculopathy . •.. Therapeutic options Surgical management (lysis of adhesion) • Selective cortisone treatment. Differential Diagnosis ............................................................................................ - Lymphoma

Tumor Disk prolapse

Selected References Petrie JL Use of ADCON-L to inhibit postoperative toms following

lumbar

disc surgery:

peridural

a preliminary

fibrosis and related symp-

report.

Eur Spine J 1996:

5

(Suppll): SIO-17 Vogelsang JP: Recurrent pain after lumbar discectomy:

the diagnostic value of peridural

scar on MRI.EurSpine J 1999: 8: 475-479

275

Peridural Fibrasis Flg.7.6 Post right laminectomy. MR image of l3 (axial, T1). Excessivefibrotic scarring (hypointense) leading to spinal stenosis.

276

Definition ............................................................................................ Rapid progressive degeneration of the segments adjacent to the fusion sites. The altered biomechanics in these adjacent segments lead to excessive stresses and segmental overloading. The mechanical overloading causes hypermobility of the segments adjacent to the fusion sites. Imaging SIgns ............................................................................................ • Modality of choice MRI: - Sagittal: Tl. T2. - Axial: n. ••. General

Degenerative disk disease and osteoarthritis of the facet joints. costovertebral joints, and costotransverse joints. • Radiographic findings Chondropathy (loss of height in the disk interspaces. disk calcification) • Degenerative disk disease and facet joint osteoarthritis (marginal irregularities. subchondral sclerosis. irregular articular surfaces) • Spondylosis deformans (marginal osteophytes: watch out for stenosis of the neural foramina and spinal canal). • MRIand CTfindings Dehydration and/or loss of height in the disk interspaces • Modic I-III (MRI) bone marrow changes. Facet joint osteoarthritis Uoint effusion, marginal osteophytes. thickening of the ligamenta naval • Degenerative disk disease and facet joint osteoarthritis (marginal irregularities. subchondral sclerosis. irregular articular surfaces) • Spondylosis deformans (marginal osteophytes; watch out for stenosis of the neural foramina and spinal canal). Clinical Aspects ............................................................................................ • Typical presentation Rapidly progressive segmental pain. Segmental neuropathy. • Therapeutic options Physical therapy (muscle strengthening exercises. proprioceptive training) • osteoporosis therapy. Differential Diagnosis ............................................................................................ Functional segmental fusion (not postoperative condition) with secondary degeneration

277

Rapidly Progressive Osteaarthritis (After Intersegmental

Fusion)

Fig. 7.7

Conventional lateral radiograph of the cervical spine. Spine is extended. Surgical fusion of C4-C5. Degenerative disk disease at C5-C6.

Fig. 7.8

MR image of the cervical spine (sagittal. T2). Marked degenerative disk disease in the adjacent segments after fusion at level C4-C5.

Selected References Chen WJ. Surgical treatment of adjacent instability after lumbar spine fusion. Spine 2001; 26: E519-524 Eck Jc. Adjacent-segment degeneration after lumbar fusion: a review of clinical. biomechanical, and radiologic studies. Am] Drthop 1999: 28: 336-340 Ghiselli G. Adjacent segment degeneration

2004: 86-A: 1497-1503

278

in the lumbar

spine.

J

Bone Joint Surg Am

MR image of (4-(5 (axial. 12). Significant posterolateral osteophytes and hypertrophic facet joint osteoarthritis with bony narrowing of the neural foramina. Fig.7.9

MR image of (4-(5 (axial. T2). Marked progression of the degenerative changes in the same segment as in Fig. 7.9 14 months later.

Fig.7.10

279

Definition

............................................................................................

Segmental stabilization with implants in fractures or spondylolisthesis (pedicle screws, wire cerclage, plate fixation, Harrington rods) and prosthetic disks. The aim is to eliminate diskogenic pain by restricting mobility. Complications: Loosening, implant fracture, displacement, accelerated degeneration of adjacent segments. Infection and skin problems' Nonunion or delayed union in patients with osteoporosis. diabetes mellitus, or infections, and in smokers and patients on steroids • Segmental overloading. abnormal stresses (trauma).

Imaging Signs

............................................................................................

~ Modality of choice Conventional radiographs. CT(MRI for neural structures) • MRIshows artifacts. ~ General Comparison with previous images is helpful in evaluating conventional radiographs (screening studies) • Multidetector CTallows multiplanar reconstruction with significantly reduced artifacts). ~ Radiographic findings Implant fracture, displacement (comparison with previous images is helpful) • Loosening (radiolucent halo. stress views). ~ CTfindings Allows evaluation of bony structures and the bone-implant interface in particular (signs of loosening) • Complex and multisegmental stabilization procedures are well visualized. Multidetector CT reduces metal artifacts: multi planar reconstruction

without step artifacts.

~ MRI findings Neural structures (compression) • Soft tissue changes (innammation) • Spin echo sequences reduce the susceptibility artifacts associated with metal. • Nuclear medicine Hot spot (implant loosening. innammation, pseudarthrosis).

Clinical Aspects

.......................................................................

~ Typical presentation Usually asymptomatic' gia.

'

Segmental pain with motion (pseudarthrosis)'

Differential Diagnosis

............................................................................................

Inflommatory changes

280

- III-defined osteolytic areas

. Neural-

Complications

of Spinal Instrumentation

Fig.7.11 Conventional A-P radiograph of the thoracolumbar spine. Harrington rod in situ after reduction of L1 fracture. Normal findings.

Fig.7.12 Conventional lateral radiograph of the upper cervical spine. Posterior cerclage wire encircling the spinous processes and bone graft. Normal findings.

281

Complications of Spina/Instrumentation

d' '" ."O

a

~.

~ o

Fig.7.13 CT (axial). Traumatic avulsion of the left pedicle. treated by open reduction and internal fixation with pedicle screws. The spinal canal is slightly widened. Both screws lie within the cancellous bone. The right screw is surrounded by a widened space with a sclerotic rim indicativeof chronicimplant loosening.

*

;;:

Fig. 7.14 Conventional lateral radiograph of the cervical spine. Multisegmental posterior and anterior stabiliza-

tion of the cervical spine.

282

Complications of Spinal Instrumentation Fig. 7.15 Conventional A-P radiograph of the lumbar spine. Typical position of pedicle screws in lumbosacral fusion.

Fig.7.16 Conventional lateral radiograph of the lumbar spine. The pedicle screws typically lie within the cancellous bone dose to the endplates.

283

Complications ~ '"

o

1:3

a

...,. ~. ~ o

of Spino/Instrumentation

Fig.?17 0 of the lumbar spine (lateral multidetector 0). Multiplanar reconstruction with minimal artifacts allowing excellent evaluation of implants in situ. Osteoporotic l4 vertebra with compressian fracture. Pedicle screws are too long and extend beyond the anterior margin of the vertebral body.

~ <;!

Fig. 7.18 Conventional lateral radiograph of the lumbar spine. Posterior lumbar interbody fusion (PLlF).The superior screw has fractured. This is one of the most common complications of posterior instrumentation.

284

Complications

of Spino/Instrumentation

fig. 7.19 Conventional lateral radiograph of the lumbar spine (detail). Anterior lumbar interbody fusion (AUF) in disk degeneration. Normal postoperative findings. with the upper screw in an atypical posi· tion.

fig. 7.20 Conventional A-P radiograph of the lumbar spine (detail). AUF: usual postoperative findings.

285

Complications

of Spino/Instrumentation

fig. 7.21

MR image of the lumbar spine (sagittal. T1 with contrast). Abscess sec-

ondary

to infection

stabilization of L3.

following

posterior

Fig. 7.22 Conventional lateral radiograph. Titanium endplates with prosthetic disks. Cementless implantation. Mobility is maintained.

and the patient

is free of

pain.

Selected

References

Lowery GL The significance of hardware failure in anterior cervical plate fixation. Patients with 2- to 7-year follow-up. Spine 1998: 23: 181-186: discussion 186-187 Slone RM. Spinal fixation. Part 3. Complications of spinal instrumentation. Radiographies 1993: 13: 797-816

286

Definition ............................................................................................ • Epidemiology More common in females than in males (4: 1) • Affects 12%of the population. 64% of postmenopausal women have vertebral fractures. • Etiology, pathophysiology, pathogenesis Metabolic disease with thinning of the trabecular structure and cortex, and reduced bone mass and density. This leads to microscopic and macroscopic insufficiency fractures. fractures as a result of trauma that does not usually cause bony injury. The disorder primarily affects the axial skeleton. Predilection for the thoracic spine. Typical findings include flattened and biconcave "fish" vertebrae. Age-related (senile form). estrogen deficiency. acromegaly. Cushing syndrome. corticosteroids. heparin. calcium phosphate deficiency. alcoholism. Imaging Signs ............................................................................................ • Modality of choice Early diagnosis: Bone density measurement with DEXA - T-score: -1 to -2.5 - osteopenia. - T-score: < -2.5 - Osteoporosis and fractures. - T-score: < -2.5 and fractures - manifest osteoporosis. Conventional radiographs: - Demonstration

of a fracture is diagnostic.

CT: - Reduced bone density is better visualized. MRI:

- In uncertain cases (possible metastases). • Radiographic findings There is loss of bone mass (> 40%) with greatly increased radiolucency. Thinning of the cancellous bone (loss of secondary trabeculae). cortical thinning • Impression fractures of the endplates (vertebral deformity) • Microscopic and macroscopic fractures (insufficiency fractures) • Compression fractures with or without displacement. spinal stenosis. and biconcave "fish" vertebrae. Kypho-

sis. • CTfindings Extent of fracture displacement. Q-CTallows quantitative bone density measurement. • MRI findings Differentiating osteoporotic from metastatic vertebral collapse. Acute vertebral collapse: - Deformation. - Diffuse bone marrow edema. - Fluid sign.

287

Senile and Postmenopausal Osteoporosis

Fig. 8.1

Conventional lateral radiograph of a vertebral specimen showing normal bone structure.

Fig.8.2 Conventional lateral radiograph of a vertebral specimen showing osteoporotic bone structure (thinning of the

cancellous bone with loss of secondary trabeculae emphasizes the longitudinal trabeculae). Flg.8.3 Conventional lateral radiograph of the lumbar spine (detail). Vertebral compression fracture with posterior displacement and spinal stenosis.

2BB

Senile and Postmenopausal

Osteoporosis

Fig.8.4 Types of vertebral compression. Normal

Wedge

Biconcave

Chronic vertebral collapse:

- Osteoporotic: fatty marrow conversion. - Metastatic: Hyperintense on T2-weighted ed images. enhancing. Diffusion-weighted sequence: - Increased diffusion coefficient.

images. hypointense on Tl-weight-

Clinical Aspects ............................................................................................ • Typical presentation Pain. Increasing kyphosis. Neurologic deficits including paraplegia. urinary excretion of hydroxyproline .

Increased

• Therapeutic options Regular exercise and load bearing (gymnastics etc.) • High mineral and vitamin diet. Bisphosphonate. calcitonin. Osteoprotegerin therapy may be an option in the future. Surgical options include vertebroplasty and correction of kyphosis • Caurian: Rapid progressive osteoarthritis and/or additional fractures after kyphoplasty or vertebroplasty.

289

Senile and Postmenopausal Differential

Osteoporosis

Diagnosis

Hyperparathyroidism

- Clinical findings

- Subperiosteal bone resorption and erosion - Schmorl nodes - Fingers affected most severely Renal osteodystrophy

Selected

- Combination of hyperparathyroidism. sclerosis. and osteomalacia - "Rugger jersey" or "rugby shirt" spine (horizontal banding)

References

Oamilakis J et .11.An update on the assessment or osteoporosis using radiologic techniques. Eur Radiol Nov 28. 20061 Epub ahead of printl Grampp S. Radiology of Osteoporosis. Berlin: Springer 2003

290

Definition ............................................................................................ •

Epidemiology Affects 3-4% of adults over 40 years. More common in men than in women (3:2). • Etiology, pathophysiology, pathogenesis Synonym: Osteitis deformans. Chronic metabolic disorder (bone remodeling disorder) • Possible viral etiology. Increased familial incidence. More com-

mon in the Anglo-Saxon population. Spinal involvement occurs in 30-75% of cases (in order of decreasing frequency: pelvis and spine, femur, and skull • Monostotic or polyostotic. Predilection for lumbar spine. Three phases: Lytic or acute phase, mixed phase, and "burned out" or sclerotic phase. Imaging Signs ............................................................................................ •

Modality of choice

Conventional radiographs, MRI: Only indicated with neurologic symptoms or suspected sarcomatous degeneration « 1% osteosarcoma and malignant fibrous histiocytoma) • Detects soft tissue tumor, necrosis. and metastases. • General

Enlarged vertebra with coarse, irregular trabecular structure • Occasionally "ivory" vertebra. •

Radiographic

findings

Enlarged vertebra with abnormally coarse structure (early forms include osteoporosis and lysis). Sclerosis, which may include an "ivory" vertebra. Secondary degenerative changes in the vertebra. Strictly segmental involvement. • CTfindings

Active (lytic) phase with enhancement after contrast administration. •

MRI findings T1

- Hypointense irregularity. T2:

- Active lesions (lytic fibrovascular areas) appear hyperintense. _ In the "burned out" phase, sclerotic and fibrotic lesions appear hypointense. There may also be fatty marrow conversion, Tl with contrast: - Active phase shows marked enhancement after contrast administration. Intensity of enhancement correlates with disease activity . ••. Nuclear medicine

Markedly increased uptake in the lytic (acute) and mixed phases.

Uptake corre-

lates with disease activity.

291

Paget Disease

s:

g

0-

~

Fig.8.5 Conventional lateral radiograph of the lumbar spine. L2 is significantly denser and slightly enlarged. It has a coarse trabecular structure.

o ;;;. o

a. •• ~

Clinical Aspects

............................................................................................

• Typical presentation Dull bone pain. Often asymptomatic. Rarely there are associated neurologic symptoms (radiculopathy). • Therapeutic options Bisphosphonates and calcitonin. • Course and prognosis Prognosis is poor with sarcomatous degeneration, otherwise excellent.

Differential Diagnosis Vertebra with hemangioma

- Usually no increase in volume

"Ivory" vertebra in lymphoma

- No stranded

Selected

or striped

pattern

References

FreyschmidtJ. Skelerrerkrankungen. Berlin: Springer 1997 Mirra JM et al. Paget's disease of bone: review with emphasis on radiologic features. Skeletal Radiology 1995; 24: 163-184 Sundaram M. Imaging of Paget's disease and fibrous dysplasia of bone. J Bone Miner Res 2006; 21(SuppI2): 28-30

292

Definition ............................................................................................ Proliferation of epidural fatty tissue. usually affecting several segments. Causes include obesity. chronic cortisone therapy (steroid abuse). Cushing syndrome. and idiopathic occurrence. Predilection for posterior thoracic spine and anterolateral lumbar spine.

Imaging Signs ............................................................................................ o Modality of choice MRI - Sagittal: n. TI. - Transverse: Tl. TI. o CTfindings Proliferation of fatty tissue in the spinal canal with displacement and posterior or occasionally anterior compression of the dural sac. o MRI findings Proliferation of structures isointense to fat in the epidural space with deformation of the dural sac and/or spinal cord ("V" shape) • The nerve roots in the foramina are completely surrounded by extradural fat. - n: Hypointense CSF is replaced by hyperintense fatty tissue. _ TI: Missing (bright) CSF signal in the compressed dural sac. increased signal in the spinal cord with compressive myelopathy. Clinical Aspects

............................................................................................ o Typical presentation Radicular pain. Unilateral or bilateral paresthesias • Spinal claudication with spinal stenosis. Cauda equina syndrome. o Therapeutic options Weight loss. Reduction or cessation of steroid therapy. Progressive neurologic symptoms are treated by surgical decompression with laminectomy.

Differential Diagnosis ............................................................................................ Primary and secondary

spinal tumors

- Inhomogeneous

enhancement

Epidural abscess

- Associated bony changes - Thickened meninges - Elevated inflammatory markers

Spinal canal lipoma

- Intradural - At least partially encapsulated

293

Fig.8.6 Body builder (chronic steroid user) complaining of increasing weakness in the lower extremities. MR image of the thoracolumbar spine (sagittal. T1) shows a thick layer of epidural fatty tissue.

Fig.8.7 MR image of T12 (axial. T1). Excessive epidural fat narrows the spinal canal.

Selected References Cera BTet al. Symptomatic spinal epidural lipomatosis without exogenous steroid intake. Neuroradiology 1989; 31; 190-192 Hierholzer Jet al. Epidural lipomatosis: case report and literature review. Neuroradiology 1996;38: 343-348 Robertson SCet al. Idiopathic spinal epidural lipomatosis. Neurosurgery 1997: 41: 68-74

294

atlantodental subluxation, rheumatoid arthritis 134. 135 atlas, fracture classification 60.61

A abscess epidural,

see epidural

abscess

epidural hematoma 261 paravertebral 164 psoas 171 acquired hydromyelia, V5. Arnold-Chiari malformation 3 acute transverse myelitis 182-185 V5. spinal multiple sclerosis 189 V5.

Anderson

and d'Alonzo

classification,

dens fractures 48 aneurysmal bone cyst 204-207 V5. giant cell tumor 211 V5. osteoblastorna 200 V5. osteoid osteoma 197 ankylosing spondylitis 147-151 V5. diffuse idiopathic skeletal hyperostosis 132 rractures 154-157 V5. Klippel-Feilsyndrome 28 and kyphosis 30 ligament calcification and bamboo spine 152.153 vs. psoriatic spondyloarthropathy 143 V5. Reitersyndrome 146 V5. Scheuermann disease 35 stress fractures 83-86 annulus fibrosus 87 defined 100 anterior lumbar interbody fusion (All F) 285 anterior subluxation 73-75 arachnoiditis 178-181 vs. granulomatous inflammation 177 Arnold-Chiari malformation 1-3 arterial spinal cord infarction 266-269 arteriovenous malformation 262-265 arthritis juvenile rheumatoid, vs. Klippel-Feil syndrome 28 rheumatoid 133-137 and chronic trauma 138-140 astrocytoma 252-255 vs. acute transverse myelitis 185 vs. ependymoma 251 vs. hemangioblastoma 258 vs. spinal multiple sclerosis 189 asymmetry, facet joint, vs. malrotation 42

B Baastrup disease 121.122 bacterial spondylitis acute 158-165 frequency distribution 167 vs. tuberculous spondylitis 169 bamboo spine 152.153 Bechterew disease 147 bone marrow inhomogeneity, vs. bone metastasis 221 bone metastases 216-221 breast carcinoma. metastasis 217 Brodie's abscess, vs. osteoid osteoma 197 bronchial carcinoma. metastasis 219 Brown-Sequard syndrome 254 bulge/buiging. disk 100.101.103-107 defined 100 burst fracture 44, 54-57 vs. Chance fracture 59 with fissure fracture 54 butterfly vertebra 21

c calcium pyrophosphate disease, vs. Baastrup disease 122 cartilaginous nodules, vs. Scheuermann disease 35 cavernous malformation, intramedullary, vs. arteriovenous malformation 265 cerclage wire 281 cerebellar tonsils, descent, vs, ArnoldChiari malformation 3 cerebrospinal fluid ((SF) fistula 272-274 cervical spine rat (2 sign 63 flexion fracture 51-53 rheumatoid arthritis 134 trauma, offset sign 61 Chance fracture 58,59 chondrosarcoma vs. chordoma 228 vs. osteochondroma 203 chorda remnant. vs. disk degeneration 89 chordoma 226-228

295

Index classification anterior subluxation

73

spinal cord trauma 66 cleavage fracture 44 cleft vertebrae 21 Codman triangle 229 colon carcinoma. metastasis compression

218

fracture

Chancefracture 59 osteoporotic 46. 288 V5. Scheuermann disease 35 concussion. spinal 66 congenital malformations 1-42 vertebral. V5. uncovertebral osteoarthritis 116 contusion. spinal 66 cord. tethered 9 Currarino triad 13 curtain sign 259 Cushing syndrome 293 cyst root canal. V5. synovial cyst 119 synovial 118,119 V5.

D degenerative changes. spine, vs. rheumatoid arthritis 137 degenerative disk disease 87-89 and gas release 108 Modic I 90-92,98 Modic II 93-95,98,127 Modic 111 (spondylosis deformans) 96-99 subchondral changes 98 degenerative spinal stenosis 126-130 Denis classification 43. 58

dens destruction. in rheumatoid arthritis 135.136 fracture 48-50 rheumatoid arthritis 134 Devic disease 189 diastematomyelia 6-8 diffuse idiopathic skeletal hyperostosis (DISH) 132,143 vs. ankylosing spondylitis 151 vs. spondylosis deformans 99 disk bulge. V5. disk herniation 102

Z96

disk calcification 108-110 disk degeneration, see degenerative disk disease disk herniation 100-102, 104 V5. Baastrup disease 122 definition. American Society of Neuroradiology 100 V5. epidural abscess 174 V5. meningioma 247 vs. synovial cyst 119 diskitis V5.

disk herniation

102

vs. Klippel-Feil syndrome 28 disk narrowing 160,161.168 dislocation, cervical spine 51 disseminated encephalomyelitis. V5. acute transverse myelitis 185 distraction injury, V5. Chancefracture 59 double railroad track sign 152 drop metastases 240 vs. tethering 12 dural sac.empty 178.180 dysraphism, spinal 16 VS. meningocele 20

E Edgren-Vaino sign 33 Effendi classification,

hangman'sfracture 63 eggshell appearance 204 Ehlers-Danlos syndrome. vs. scoliosis 39 empty thecal sac 178,180 encephalomyelitis. disseminated. vs. acute transverse myelitis 185 eosinophilic granuloma. vs. Ewing sarcoma 231 ependymoma 248-251 vs. astrocytoma 255 vs. hemangioblastoma 258 vs. nerve sheath tumor 239 vs. spinal multiple sclerosis 189 epidural abscess 172-174 vs. bacterial spondylitis 160 vs. spinal epidural lipomatosis 293 vs. tuberculous spondylitis 169 epidural fibrosis. vs. disk bulge 107 epidural hematoma. vs. epidural abscess 174

Index

exostosis 201.202 extrusion, disk 103

fusion physiologic, vs. dens fracture spinal. surgical 28 vertebral. acquired 25

F

G

facetectomy, partial, vs. spondylolisthesis 82.125 facet joints ankylosis 153 asymmetry, V5. malrotation 42 degeneration 111-115 dislocation 73 osteoarthritis 111

ganglioglioma, vs. astrocytoma 255 gas release. in disk degeneration 108 giant cell tumor 208-211 vs. aneurysmal bone cyst 207 vs. chordoma 228 vs. Langerhans cell histiocytosis 214 gibbus 30.31. 34 granulomatous infections, spinal cord 175-177 Guillain-Barre syndrome vs. arterial spinal cord infarction 269 vs. epidural abscess 174

Ewing sarcoma V5. Langerhans

229-231 cell histiocytosis

214

failed back surgery syndrome

270.271 fat (2 sign 63 fibrosis epidural. vs. disk bulge 107 peridural 275. 276 fibrous histiocytoma, malignant, vs. chordoma 228 filum terrninale ependymoma

50

H 251

V5. nerve sheath tumor 239 nexion fracture. cervical spine 51-53 Foix-Alajouanine syndrome. vs. arterial spinal cord infarction 269

foraminal stenosis 114 Forestier disease 131

vs. ankylosing spondylitis 151 V5. psoriatic spondyloarthropathy see also diffuse idiopathic skeletal hyperostosis fractures ankylosing spondylitis 154-157 causes 45-47 classification 43.44 vs. facet joint degeneration 115 insufficiency 138 sacrum 76-78 vs. osteoid osteoma 197 stress, in ankylosing spondylitis 83-86 vertebral vs. Modic I degenerative disk disease 92 vs. Modic II degenerative disk disease 93 fungal infection, vs. tuberculous spondylitis 169

143

hangman's fracture 63-65 Harrington rod 280.281 hemangioblastoma 256-258 vs. arteriovenous malformation 265 vs. ependymoma 251 hemangioma 190-194 atypical. vs. Modic Idegenerative disease 92 vs. Modic II degenerative disk disease 93 vs. multiple myeloma 225 vs. Paget disease 292 hematoma. epidural 259-261 vs. epidural abscess 174 hemivertebra, lateral 21 hemorrhage, spinal cord, vs. spinal cord trauma 68 herniation, defined 100 histiocytoma, vs. chordoma 228 histiocytosis, see Langerhans cell histiocytosis Horner's syndrome 269 hydromyelia acquired, vs. Arnold-Chiari malformation 3 vs. diastematomyelia 8 hydrops fetalis 15 hypernephroma, metastasis 218

disk

297

Index hyperostosis nowing 132 skeletal. diffuse idiopathic (DISH) 131-132 hyperparathyroidism. V5. osteoporosis 290

L Langerhans cell histiocytosis vs. Ewing sarcoma 231 leptomeningeal metastases vs. arachnoiditis 181

vs. ependymoma

212-214

251

vs. granulomawus inflammation leptomeningitis 175

ligamenta nava. hypertrophy

fracture 44 infarction. spinal vs. acute transverse myelitis arterial 266-269 impaction

V5.

spinal multiple

ligament calcifications

sclerosis

nava hypertrophy

189

120

lipoma, spinal canal, vs. spinal epidural

V5.

Langerhans cell histiocytosis

V5.

rheumatoid arthritis

vs. facet joint degeneration 115 V5. osteoid osteoma 197 inflammatory disorders 133-189 instrumentation, complications

280-286 insufficiency

fracture

lipomatosis

214

137

inflammation

138

ivory vertebral body 291.292

293

lipomatosis spinal, vs. epidural hematoma

261

spinal epidural

293.294 liposarcoma, vs. Modic II degenerative disk disease 93 lumbarization 4, 5 lumbar radiculopathy, fracture of sacrum

lymphoma

76-78

intradural tumor. VS. arachnoiditis 181 intramedullary tumor YS. acute transverse myelitis 185 V5. granulomatous inflammation 177

vs. insufficiency 78

232-236

vs. bone metastasis

vs. chordoma

221

228

vs. Langerhans cell histiocytosis vs. Pager disease 292

232. 233. 236. M Magerl classification, spinal injury

J

43.44

Jefferson fracture juvenile

60-62

rheumatoid

malformations

arthritis

137

vs. Klippel-Feil syndrome

28

arteriovenous congenital

vertebral K kissing spine 121.122 Klippel-Feil syndrome Knutsson sign

kyphosis

26-28

29.33

29-32

osteoporotic 30. 32 vs. Scheuermann disease tuberculous 35

262-265 1-42

21-25

malrotation 40-42 Marfan syndrome, vs. scoliosis meningioma 244-247 vs. nerve sheath tumor 239 meningocele 16-20

metabolic disorders

287-294

39

metastases 35

vs. aneurysmal vs. arachnoiditis vs. astrocytoma

bone cyst

207

181 255

vs. bacterial spondylitis breast carcinoma 217 bronchial carcinoma 219

298

99

ligament ossification, vs. ligamenta

infection

sacrum

120.127

152,153

vs. spondylosis deformans

185

177

160

214

Index nucleus pulposus defined 100

V5. chordoma 228 colon carcinoma 218 drop 240 V5. tethering 12 V$. V5.

ependymoma 251 epidural hematoma

o 261

vs. giant cell tumor 211 V5. granulomatous inflammation 177 vs. hemangioma 194 hypernephroma 218 V5. insufficiency fracture of sacrum V5.

87

Langerhans cell histiocytosis

78 214

leptomeningeal and intramedullary 240-243 VS. meningioma 247 VS. multiple myeloma 225 V5. osteoblastoma 200

osteogenic, vs. spondylolisthesis 82 V5. osteoid osteoma 197 prostate carcinoma 217 V5. tuberculous spondylitis 169 see also bone metastases Meyerding classification. spondylolisthesis 79.81. 123. 126 multiple sclerosis V5. astrocytoma 255 vs. granulomatous inflammation 177 vs. metastasis 243 spinal 186-189 myelitis acute transverse. V5. granulomatous inflammation 177 vs. arterial spinal cord infarction 269 myeloma. multiple 222-225 myelomeningocele 16-20 vs. kyphosis 29 vs. sacrococcygeal teratoma 15 N necrosis, spinal cord, vs. arterial infarction 269 nerve sheath tumors 237-239 neurapraxia 66 neuroblastoma, vs. Ewing sarcoma 231 neurofibroma, vs. meningioma 247 neurofibromatosis, vs. scoliosis 39 neuromyelitis optica 189 notochord, persistent 21 vs. hemangioma 194

odontoid process, see dens offset sign, cervical spine trauma 61 onion peel appearance 229 os odontoideum, vs. dens fracture 50 ossification, ligament, vs. ligamenta flava hypertrophy 120 ossified posterior longitudinal ligament, vs. spondylosis deformans 99 osteitis deformans 291 osteoarthritis facet joints 111 rapidly progressive, after intersegmental Fusion 277-279 uncovertebral 116,117 osteoblastoma 198-200 vs. aneurysmal bone cyst 207 vs. osteoid osteoma 197 osteochondroma 201-203 osteodystrophy, renal. vs. osteoporosis 290 osteogenesis imperfecta, vs. scoliosis 39 osteogenesis imperfecta tarda 35 osteoid osteoma 195-197 vs. osteoblastoma 200 osteolysis, in bacterial spondylitis 161 osteomyelitis vs. Ewing sarcoma 231 vertebral body. vs. epidural abscess 174 osteoporosis VS.bone metastasis 221 fractures, vs. metastatic fractures 46 and kyphosis 30.32 vs. multiple myeloma 225 senile and postmenopausal 287-290 osteosarcoma vs. Ewing sarcoma 231 parosteal, vs. osteochondroma 203

p pachymeningitis. VS. (SF fistula Paget disease 291. 292 pannus tissue, in rheumatoid arthritis 135. 136

274

299

Index parasyndesmophytes, V5. spondylosis deformans 99 paravertebral abscess 164 pedicle screws 280.282-284 peridural fibrosis 275. 276 plasmacytoma 222 vs. bone metastasis 221 vs. chordoma 228 polyneuropathy, postinfectious. vs. epidural abscess 174 posterior lumbar interbody fusion (PUF) 284 postmenopausal osteoporosis 287-290 postoperative disorders 270-286 prolapse use of term 100 see also disk herniation prostate carcinoma. metastasis 217 prosthetic disks 280. 286 protrusion. disk 103-107 see a/sa bulge/bulging pseudarthrosis V5. dens fracture 50 and stress fractures 83-85 pseudospondylolisthesis 81.82.109. 123-125.128 pseudosubJuxation. V5. hangman's fracture 65 psoas abscess 171 psoriasis vs. ankylosing spondylitis 151 V5. Reiter syndrome 146 psoriatic spondyloarthropathy 141-143

R radiculopathy. lumbar. V5. insufficiency fracture of sacrum 78 railroad track sign 152 Reiter syndrome 144-146 vs. ankylosing spondylitis 151 renal osteodystrophy, vs. osteoporosis 290 rheumatoid arthritis 133-137 and chronic trauma 138-140 juvenile. vs. Klippel-Feil syndrome 28 vs. psoriatic spondyloarthropathy 143 vs. Reiter syndrome 146 subluxation, vs. dens fracture 50 root canal cyst, vs. synovial cyst 119

300

rotation, with scoliosis. V5. malrotation 42

5 sacralization 4, 5 sacrococcygeal teratoma 13-15 sacroiliitis 144 vs. insufficiency fracture of sacrum 78 sacrum, insuffiCiency fracture 76-78 saddle anesthesia 128.179 salt and pepper pattern \91 sarcoidosis 175, 176 vs. arachnoiditis 181 vs. spinal multiple sclerosis 189 sarcoma. see Ewing sarcoma scalloping. vertebral body 237 Scheuermann disease 33-35 and disk degeneration 87 vs. kyphosis 29 vs. scoliosis 39 Schmorl node 33.87.88.110.127 schwannoma vs. disk bulge 107 vs. ependymoma 25\ vs. meningioma 247 sclerosis, subchondral 109 sclerotic bone islands vs. osteoblastoma 200 vs. osteoid osteoma 197 scoliosis 36-39 vs. Baastrup disease 122 classification 36 with rotation, vs. malrotation 42 seat belt fracture 58,59 senile osteoporosis 287-290 sequestration, disk 103.105 sequestrum, vs. osteoid osteoma 197 shear fracture 44 vs. Chance fracture 59 shock. spinal 66 skeletal hyperostosis. see diffuse idiopathic skeletal hyperostosis spinal cord granulomatous infections 175-177 severed, vs. spinal cord trauma 68 spinal cord hemorrhage. vs. spinal cord trauma 68 spinal cord trauma 66-68 spinal dysraphism 16 vs. meningocele 20

Index spinal fusion, surgical. vs. Klippel-Feil syndrome 28 spinal infarction acute, V5. spinal multiple sclerosis acute transverse myelitis

V5.

189

185

vs. astrocytoma

255 243 spinal Injury 43-86 Magerl classification 43.44 spinal instrumentation. complications 280-286 spinai multiple sclerosis 186-189 spinal stenosis 192 degenerative 126-130 nondiskogenic vs. disk bulge 107 V5.

metastasis

vs. disk herniation

102

spine. kissing 121. 122 spondylarthritis 111.112.114 and synovial cyst 118 spondylitis ankylosing. see ankylosing spondylitis anterior 147.149.150 bacterial. see bacterial spondylitis V5. Modic I degenerative disk disease 92 specific, vs. acute bacterial 160 vs. spondylolisthesis 125 tuberculous 165-171 spondyloarthropathy psoriatic 141-143 seronegative. vs. rheumaroid arthritis

137

spondylodiskitis 158.159.161 aseptic 147.150 V5.

epidural abscess

174

Modic I degenerative disk disease 92 vs. stress fractures 83

V5.

tuberculous

spondylolisthesis

stenosis neural foramina 99. 114 vs. disk bulge 107 vs. disk herniation 102 spinal canal 26.40.52.56.99. 120.192 degenerative 126-130 vs. disk bulge 107 VS. disk herniation 102 Still disease 137 stress fritctures, in ankylosing spondylitis 83-86 stress phenomena 79-82 subchondral sclerosis 109 subdural synostosis, VS. dens fritcture 50 subluxation anterior 73-75 atlantodental, rheumatoid arthritis 134. 135 cervical spine 51 vs. dens fracture 50 traumatic, vs. rheumittoid arthritis 140 surgery, postoperative disorders 270-286 syndesmophytes 147-149 VS. spondylosis deformitns 99 synostosis, subdural. VS. dens fracture 50 synovial cyst 118. 119 syringobulbia 69 syringohydromyelia 69-72 systemic lupus eryrhemittosus, vs. spinal multiple sclerosis 189

175

79-82. 123-126

Meyerding classification

79.81

spondylolysis 79 healed. vs. spondylolisthesis 82 spondylosis. V5. diffuse idiopathic skeletal hyperostosis 132 spondylosis deformans (Modic III) 96-99 Sprengel deformity 27 squaring. vertebral body 147.148.154 staging classification, sacrococcygeal teratoma 13

T teardrop fracture, cervical spine 51, 52 teratoma, sacrococcygeal 13-15 tethering 9-12 post-traumittic 71 recurrent 19 thecal sac. empty 178.180 tonsils. cerebellar. descent 3 tram tracking 214 transverse myelitis, acute 182-185 vs. astrocytoma 255 vs. granulomatous inflammation 177 vs. metastitsis 243 vs. spinal multiple sclerosis 189 301

Index trauma V5.

Baastrup disease

122

chronic. and rheumatoid arthritis 138-140 V5. malrotation 42 vs. spondylolisthesis 125 traumatic subluxation, arthritis 140

V5.

rheumatoid

tuberculosis 175 tuberculous spondylitis 165-171 tuberculous spondylodiskitis 175 tumors 190-258 V5. aneurysmal bone cyst 207 V5. degenerative spinal stenosis 128 intradural, vs. arachnoiditis intramedullary

181

acute transverse myelitis 185 granulomatous inflammation 177 nerve sheath 237-239 primary, V5. osteoblastoma 200 V5. sacrococcygeal teratoma 15 V5. spinal epidural lipomatosis 293 vs. syringohydromyelia 72 V5.

V5.

u uncovertehralosteoarthritis

116,117

v vacuum phenomenon

108-110

vascular disorders 259-269 vasculitis, vs. arterial spinal cord infarction 269

302

venous plexus, enlarged, vs. (SF fistula 274 vertebra cleft 25 collapse 289 vs. bone metastasis 221 vs. multiple myeloma 225 vs. spondylosis deformans 99 compression, types 289 fractures vs. bacterial spondylitis 160 causes 45-47 vs. tuberculous spondylitis 169 fusion acquired 25 congenital 21.25 malformations 21-25 waist 25. 27. 28 vertebral body ivory 232.233.236.291.292 osteomyelitis, vs. epidural abscess 174 scalloping 237 sequestrum 165 squaring 147.148.154 vertebra plana 35.212-214 von Hippel-Lindau disease 256.257

w waist. vertebral 25.27.28 wedge fracture, cervical spine 51, 52 Wegener granulomatosis 175,176